LIB RARY OF CONGR ESS, 



Shelf 



•mm 



UNITED STATES OF AMERICA. 



THE DISEASES OF 
THE NERVOUS SYSTEM 



A TEXT-BOOK 
FOR PHYSICIANS AND STUDENTS 



Dr. LUDWIG HIRT 

PROFESSOR AT THE UNIVERSITY' OF BRESLAU 



TRANSLATED, WITH PERMISSION OF THE AUTHOR, BY 

AUGUST HOCH, M. D. 

ASSISTED BY 

FRANK R. SMITH, A. M. (Cantab.), M. D. 

ASSISTANT PHYSICIANS TO THE JOHNS HOPKINS HOSPITAL 

WITH AN INTRODUCTION BY 
WILLIAM OSLER, M. D., F. R. C. P. 

PROFESSOR OF MEDICINE IN THE JOHNS HOPKINS UNIVERSITY, ETC. 



WITH 178 ILLUSTRATIONS 





NEW -'YORK 


D. 


APPLETON AND COMPANY 




1893 









Copyright, 1893, 
By D. APPLETON AND COMPANY. 



Electrotyped and Printed 
at the appleton press, u. s. a. 



PREFACE. 



To add yet another to the vast number of text-books on 
nervous diseases which already exist, and most of which are 
admirably written, is a somewhat serious undertaking, and the 
question whether the want of such a book is really felt can be 
answered in the affirmative only with some diffidence. If, de- 
spite this, the author has ventured to enter the field with writ- 
ers like Erb, Eulenburg, Strumpell, Seeligmiiller, Mobius, and 
others, some responsibility must rest upon the shoulders of his 
publisher, who has more than once assured him that there is 
still room for another text-book in addition to those already in 
our libraries. He was influenced, too, by the hope that here 
and there on certain points the treatment of the subject, by 
varying from that ordinarily adopted, might while rendering 
it more easily comprehensible to the beginner make the book 
none the less reliable as an adviser to those of wider expe- 
rience. With this end in view, we have considered the manner 
of dividing the subject matter to be of no small importance, 
and have therefore chosen to discuss the diseases of the brain, 
those of the spinal cord, and those of the general nervous sys- 
tem separately, while diseases of the peripheral nerves, cra- 
nial as well as spinal, have been fully treated of by themselves. 
We shall not, as others have done before in treating of the 
cranial nerves, discuss one here, one there, and the peripheral 
nerves of the spinal cord partly in one place, partly in another, 
according as we are dealing with their motor or their sensory 
disturbances, but shall speak of the former and of the latter in 
the order that their anatomical position would indicate. In 
this way we shall be enabled to obtain a comprehensive view 
of them, which is undoubtedly highly desirable. To please all 
is impossible. Of course, one reader would wish that one 
point had been treated in this particular way and in that par- 
Cm; 



IV PREFACE. 

ticular place, while another would have fancied something to- 
tally different. About this we cherish no fond illusions. A 
systematic discussion of the sympathetic system, as well as of 
affections due to specific micro-organisms — e. g., tetanus, lyssa 
— we have not attempted, partly for other reasons, and partly 
because the space allotted to us would not allow of it. Further 
deviations from the usual course — e. g., the attempt to divide 
the functional neuroses into two classes, and to put tabes not 
among spinal diseases, but among those affecting the general 
nervous system — are sure to meet with sharp criticism, and 
we do not expect that the position we have assumed toward 
hypnotism and the treatment by suggestion will for the present 
meet with general acceptation. Every new and strange idea 
necessarily requires time to win its way and gain for itself a 
large circle of adherents. We hope it will be our pleasant task 
to record in a new edition (if such by good chance be called 
for) the assent of more of our professional brethren to this 
view. Finally, the list of references which we have inserted 
at the end of each chapter, thinking it would be of conven- 
ience to such of our readers as wish to study fully any particu- 
lar point, this list, we confess, will not bear too severe a criti- 
cism ; naturally, we could not mention every work dealing 
with the subject ; for such a task neither the knowledge of the 
author nor the capacity of the book could suffice. Only the 
most important, and of these only the more recent, works could 
be quoted. 

Only too well aware of his shortcomings, but convinced 
that he has set down concisely what he has learned from oth- 
ers and observed himself in an extensive hospital as well as 
private practice— convinced also that the illustrations, for which 
he has to thank the generosity of the publisher, will do much 
to enhance the interest of the text — the author bows willingly 
to the dictum of the old proverb, 

" Habent sua fata libelli." 

Dr. Ludwig Hirt. 

Breslau, September, 1889. 



INTRODUCTORY NOTE. 



The pleasure of introducing to the profession of this country 
a translation of a standard work is enhanced by the opportu- 
nity it affords of acknowledging how great is our debt to those 
— translators and publishers — who have made current in Eng- 
lish the works of Trousseau, Niemeyer, Virchow, Cohnheim, 
and others. All recognize the necessity of teachers knowing 
the classical works in all languages, but of equal importance is 
it that the practitioners in all countries should have easy ac- 
cess by means of translations to the thoughts and experience, 
the ways and methods, of the masters of our art the world over. 
No better corrective exists to the vice of Philistinism — that nar- 
row conceit of the special prominence of medicine in any one 
country — than a wide diffusion in all of the best works of each. 

Early in 1890 my attention was called by Dr. Weir Mitchell 
to the first part of Prof. Hirt's Handbuch der Nervenkrank- 
heiten, which he characterized as an exceptionally well ar- 
ranged and thorough work on diseases of the nervous system. 
The completed work seemed in many respects so admirable a 
text-book that I wrote to Prof. Hirt and asked his permission 
to have it translated. 

The arrangement of the subjects to which the author re- 
fers in the preface, though somewhat novel, is justifiable and 
entirely satisfactory ; and it is a distinct advance in classifica- 
tion to place tabes dorsalis and dementia paralytica among 
the diseases of the general nervous system, instead of in the 
sections on diseases of the cord and diseases of the brain re- 
spectively. 

The fact which makes the work of value to the teacher, the 
student, and the practitioner is the graphic description of the 
anatomy and symptomatology of the different diseases. Where 
all is so good it is invidious to select, but the chapter on tabes 

(v) 



vi INTRODUCTORY NOTE. 

is an illustration of our author's lucid and, at the same time, 
thorough treatment of his subject. The various affections are 
treated of also from an advanced modern standpoint ; conflict- 
ing theories and passing observations are submitted to a wise 
criticism through which the author's own large and varied ex- 
perience is very apparent. 

An attractive aspect of the work is the excellent character 
of the illustrations, which, as they are in great part original, 
will be a pleasing relief to the hackneyed cuts which have for 
so long passed from book to book in English works. 

Pursuing the via media in the important question of treat- 
ment, neither displaying the pessimism which too many mala- 
dies of the nervous system would seem to justify, nor an opti- 
mism so flagrant as to savor of quackery, Prof. Hirt is a safe 
guide in the highways and byways of neurotherapeutics. 

And, lastly, I think the author has been fairly handled by 
his translators, who, bearing in mind the admonition of Dryden, 
" not to lackey by the side of his author, but to mount up be- 
hind him," have given a clear and interesting rendering of the 
original. 

William Osler. 
Baltimore, January, i8gj. 



CONTENTS. 



PAGE 

Diseases of the Brain and its Meninges, including those of 

the Cranial Nerves i 

PART I. 

Diseases of the Meninges of the Brain 3 

Chap. I. — Inflammation of the inner surface of the dura mater, pachymeningitis 

interna hemorrhagica, hematoma duras matris ■> 
II. — Inflammations of the soft membranes of the brain, leptomeningitis, puru- 
lent meningitis .......... 9 

PART II. 

Diseases of the Cranial Nerves 23 

Chap. I. — Diseases of the olfactory nerve 24 

II. — Diseases of the optic nerve 28 

III. — Diseases of the nerves supplying the ocular muscles . . . .40 

IV. — Diseases of the trigeminal nerve ........ 52 

V. — Diseases of the facial nerve . 77 

VI. — Diseases of the auditory nerve . 94 

VII. — Diseases of the glosso-pharyngeal nerve . . . . . . . 105 

VIII. — Diseases of the vagus (pneumogastric nerve) 108 

IX. — Diseases of the accessory nerve 138 

X. — Diseases of the hypoglossal nerve ........ 142 

XI. — Simultaneous affection of several cranial nerves — Multiple paralysis of 

the cranial nerves 150 

PART III. 

Diseases of the Brain Proper 163 

I. The study of cerebral lesions with reference to their seat — Topical diagnosis 

— Doctrine of localization ......... 164 

Symptoms referable to cortical lesions ....... 166 

Symptoms referable to lesions of the white matter of the hemispheres and 

to lesions of the basal ganglia ........ 188 

(vii) 



yiii CONTENTS. 

PAGE 

II. The study of cerebral lesions with reference to their pathological nature — 

Pathological diagnosis . . . . . . . ... .211 

Affections of the brain due to disease of the blood-vessels . . . .213 

A. Diseases of the cerebral vessels and their consequences . . . 213 

1. Cerebral haemorrhage 215 

2. Embolism and thrombosis of the cerebral arteries — Encephalo- 

malacia ........... 245 

3. Endarteritis (syphilitica) 252 

4. Dilatation of the arteries of the brain 254 

5. The neuroses of the arteries of the brain (anaemia and hyperemia 

of the brain) 255 

B. Diseases of the cerebral veins and sinuses ...... 258 

Inflammatory processes of the brain substance ...... 261 

1. Purulent encephalitis — Brain abscess ....... 261 

2. Nonsuppurative encephalitis and its consequences (" athetosis ") . 267 

A. In adults 267 

B. In children — Cerebral palsy of children — Hemiplegia infantilis 

spastica — Polio-encephalitis 268 

Brain tumors 288 

Appendix — Parasites of the brain ........ 303 

Congenital diseases — Hydrocephalus — Meningocele — Porencephaly — Ab- 
sence of certain parts of the brain . . . . . . 305 

Diseases of the Spinal Cord 311 

PART I. 

Diseases of the Spinal Meninges 312 

Chap. I. — Inflammations of the dura mater — Pachymeningitis spinalis . . . 313 
II. — Inflammations of the soft spinal meninges — Leptomeningitis spinalis . 319 
III. — Haemorrhage into the spinal membranes — Meningeal apoplexy — Pachy- 
meningitis interna haemorrhagica ....... 323 

PART II. 
Diseases of the Spinal Nerves 327 

A. Diseases of the motor and sensory nerves 329 

I. Diseases of the cervical nerves 329 

Chap. I. — Lesions of the cervical plexus ...... 335 

II. — Lesions of the brachial plexus ...... 338 

II. Diseases of the dorsal nerves 360 

III. Diseases of the lumbar nerves ........ 363 

IV. Diseases of the sacral and coccygeal nerves 368 

V. Neuritis involving several spinal nerves at the same time — Multiple 

neuritis 385 

B. Diseases of the trophic and vaso-motor nerves ...... 393 

Appendix — Diseases of the muscles — Primary myopathies . . . 406 



CONTENTS. ix 

PART III. 

PAGE 

Diseases of the Substance of the Spinal Cord 416 

I. Consideration of spinal diseases with reference to their seat — Topical diag- 
nosis 416 

1. Lesions of the gray matter — Poliomyelitis ...... 422 

Chap. I. — Poliomyelitis anterior acuta — Infantile spinal paralysis . 424 
II. — Atrophia muscularis progressiva spinalis — Progressive mus- 
cular atrophy . . . . . . . . . 431 

11. Lesions of the white matter of the spinal cord — Leucomyelitis . . 435 

A. Primary lesions of the white columns 435 

B. Secondary lesions of the white columns 439 

in. Lesions of the gray and white matter of the spinal cord . . . 440 

II. Spinal lesions regarded from their pathological aspect — Pathological diag- 
nosis 451 

I. Affections of the spinal cord due to diseases of the blood-vessels . . 451 

A. Diseases of the arteries of the spinal cord and their consequences 451 

1. Spinal haemorrhage — Hgemorrhagia (or apoplexia) medulla? 

spinalis — Hsematomyelia 452 

2. Embolism and thrombosis of the spinal arteries and myelo- 

malacia 454 

3. Endarteritis (syphilitica) 454 

4. Dilatation of the spinal arteries . . . . . -455 

5. Neuroses of the spinal arteries 455 

II. Inflammatory processes in the substance of the spinal cord . . . 458 

1. Purulent myelitis— Abscess of the spinal cord .... 458 

2. The non-purulent myelitis 458 

A. The acute form 458 

B. The chronic form ......... 460 

Hi. Spinal tumors 460 

Appendix — Parasites of the spinal cord 462 

IV. Congenital diseases — Hydrorrhachis — Spina bifida .... 463 



Diseases of the General Nervous System 468 

PART I. 

Diseases of the General Nervous System without any Recognizable 

Anatomical Basis — "Functional Neuroses" 471 

First Group. — Neuroses which are wont to run their course without any essen- 
tial implication of the general organism ....... 473 

Chap. I. — Chorea — Chorea Sancti Viti — St. Vitus' dance — Ballismus — Mel- 
ancholia saltans — Sydenham's disease 473 

II. — Tetany — Tetanilla — Tetanus intermittens 484 

III. — Paralysis agitans — Shaking palsy — Parkinson's disease — Chorea 

procursiva 489 



x CONTENTS. 

PAGE 

Second Group. — Neuroses in which the entire organism is more or less severely 

implicated ............. 497 

Chap. I. — Neurasthenia — Nervous prostration ...... 497 

II. — Hysteria 506 

III. — Epilepsy — Falling sickness — Morbus sacer — Morbus comitialis . 532 
IV. — Hystero - epilepsy — Major hysteria — Hypnotism — Treatment by 

suggestion 561 

PART II. 
Diseases of the General Nervous System with Known Anatomical 

Basis 576 

Chap. I. — Multiple sclerosis — Disseminated sclerosis — Insular sclerosis — Sclerose 

en plaques — Sclerosis cerebro-spinalis disseminata sive multiplex . 576 
II. — Tabes dorsalis — Locomotor ataxia — Posterior spinal sclerosis — Leuco- 

myelitis posterior chronica 586 

III. — Dementia paralytica progressiva — General paralysis of the insane — 

General paresis — Softening of the brain 644 

IV. — Syphilis of the general nervous system . . . . . . 656 

Appendix — Intoxication paralyses 660 



LIST OF ILLUSTRATIONS. 



FIG. PAGE 

1. Cross-section through the cerebral cortex and its membranes .... 4 

2. Anterior and middle portions of the base of the brain . . . . .24 

3. Diagram showing the course of the optic fibres in the chiasm . . .28 

4. Diagram showing the origin of the optic nerve (after Wernicke) . . . 30 

5. Field of vision of the left and right eye (after Forster) 35 

6. Field of vision of the left and right eye in left-sided hemianopia (after Gow- 

ers) 36 

7. Cross-section through the region of the ant. corpora quadrigemina . . .40 

8. Diagrammatic longitudinal section through the pons with the nuclei of the 

ocular nerves (after Gowers) ......... 41 

9. Cross-section through the region of the tegmentum (after Schwalbe) . . 42 

10. Cross-section through the pons (after Schwalbe) . . .' . . -43 

11. Nuclei of the trigeminal nerve (after Schwalbe) ...... 53 

12. Cross-section through the medulla oblongata (after Schwalbe) . . .54 

13. Distribution of the sensory cutaneous nerves on the head . . . -74 

14. Diagram showing the course of the facial fibres in the pons (after Schwalbe) . 78 

15. Diagram showing the decussation of the fibres going to the extremities, and 

of those going to the face, in the pons and medulla oblongata . . .84 

16. Erb's diagram for facial paralysis ......... 88 

17. Some of the so-called " motor points " on the face and neck . . . .92 

18. Diagrammatic section through the medulla oblongata in the region of the 

(lower) olive ............ 95 

19. Cross-section through the medulla oblongata (after Schwalbe) . . . 109 

20. Bilateral paralysis of the recurrent laryngeal 115 

21. Recurrent laryngeal paralysis .......... 115 

22. Paralysis of the recurrent laryngeal on the left side . . . . . 115 

23. Paralysis of both posterior crico-arytenoids . . . , . . .115 

24. Paralysis of the right post, crico-arytenoid . . . . . . .115 

25. Paralysis of both internal thyro-arytenoids ....... 115 

26. Paralysis of both internal thyro-arytenoids . . . . . . .115 

27. Cross-section through the cervical cord ........ 138 

28. Superficial origin of the cranial nerves ........ 143 

29. Base of the skull with the emerging cranial nerves (after Henle) . . . 144 

30. Cortical centres of the left hemisphere (after Gowers) ..... 145 

31. Cross-section through the medulla oblongata (after Wernicke) . . . 145 

32. Hemiatrophia linguae 146 

33. Hemiatrophia linguae ........... 147 

34. Pharyngeal and laryngeal electrode with arrangement for making and break- 

ing the current (after Erb) 152 

(xi) 



x ii LIST OF ILLUSTRATIONS. 

FIG. PAGE 

35. Facial expressions in progressive bulbar paralysis (after Leyden, Eichhorst) . 156 

36. Cross-section through the upper portion of the medulla oblongata . . .158 

37. The posterior (dorsal) aspect of the medulla oblongata 159 

38. Right hemisphere (after Exner) 167 

39. Left hemisphere (after Exner) 168 

40. Convolutions and fissures of the lateral aspect of the brain (after Ecker) . 169 

41. Convolutions and fissures at the base of the brain (diagrammatically after Ecker) 170 

42. Convolutions and fissures of the median aspect of the brain .... 171 

43. Convolutions of the island of Reil (J. R.) made visible by removing the oper- 

culum 172 

44. Topographical relations between the exterior of the skull and the surface of 

the brain (after Ecker) 173 

45. Wernicke's schema for the cortical mechanism of speech .... 176 

46. 47. Lichtheim's schema illustrating the seven different forms of aphasia. . 179 

48. Diagram showing the direct system of fibres (Flechsig, Mendel) . . .183 

49. Course of the fibres from the internal capsule to the crus cerebri (diagram- 

matic after Wernicke and Edinger) 189 

50. Horizontal section through the hemispheres ....... 190 

51. View of the ventricles on horizontal section (after Edinger) .... 191 

52. Horizontal section through the brain, about a finger's breadth below that 

represented in Fig. 51 (Edinger) ........ 192 

53. Base of the brain (with the first portion of the spinal cord) .... 193 
54-57. So-called " frontal sections " through the brain (after Edinger) . 194, 195 
58. Points at which the Pitres-Nothnagel's sections are made .... 196 
59-64. Pitres-Nothnagel's sections 197-199 

65. Diagrammatic cross-section through the anterior corpora quadrigemina (after 

Edinger) , 2co 

66. Longitudinal section through the region of the corpora quadrigemina of a 

human foetus twenty-eight weeks old (after Edinger) .... 201 

67. Diagrammatic horizontal section through the decussation of the superior pe- 

duncles of the cerebellum (after Edinger) 202 

68. Sagittal section through pons and medulla oblongata (after Mendel) . . 203 

69. Cross-section through the region of the ant. corpora quadrigemina . . 204 

70. Diagram showing the decussation of the fibres going to the extremities, and 

of those going to the face, in the pons and medulla oblongata . . . 205 

71. The cerebellum seen from behind 206 

72. Cerebellum seen from in front 207 

73. The connections of the cerebellum 207 

74. The anterior (lower) surface of the medulla oblongata 208 

75. The posterior (dorsal) aspect of the medulla oblongata 209 

76. Diagram showing the circle of Willis 212 

77. The cortical distribution of the middle cerebral artery (after Charcot) . . 213 

78. Frontal section through the cerebral hemispheres, one centimetre behind the 

chiasm ............. 214 

79. Cerebral artery from an apoplectic focus (after Cornil and Ranvier) . . 216 

80. Miliary aneurism of a small artery of the lenticular nucleus (after Marchand) . 216 

81. The large head electrode (covered with sponge) of Erb 242 

82. Porencephaly 267 

83. Hemiatrophy of the left side of the body, front 274 

84. Hemiatrophy of the left side of the body, back 275 

85. Hemiatrophy of the left side of the body from traumatism, front . . . 276 



LIST OF ILLUSTRATIONS. 



Xlll 



FIG. PAGE 

86. Hemiatrophy of the left side of the body from traumatism, back . . . 277 

87. Atrophy of the left upper and lower extremity 278 

88. Atrophy of paralyzed side .......... 279 

89. Atrophy of paralyzed side ; contracture of wrist ...... 280 

90. Atrophy of paralyzed side ; contracture of ankle 282 

91. Atrophy of paralyzed side ; contracture of ankle 283 

92. Convulsive movements of the extremities ....... 285 

93. Glioma telangiectaticum (after Ziegler) 28S 

94. Papillary carcinoma in the third ventricle (after Ziegler) .... 289 

95. Cysticercus racemosus (after Marchand) . ....... 304 

96. Cross-section through the vertebral column and the spinal cord (diagram- 

matical) (after Eichhorst) 313 

97. Cross-section through the middle of the cervical enlargement in pachymenin- 

gitis cervicalis hypertrophica (after Charcot) . . . . . .314 

98. Position of the hand in pachymeningitis cervicalis hypertrophica (Charcot) . 316 

99. Diagrammatic outline of the cervical and brachial plexuses (after Schwalbe) . 330 

100. The superficial branches of the cervical plexus (after Hirschfeld and Le- 

veille) 331 

101. Deep dissection of the axilla, showing the brachial plexus (after Hirschfeld 

and Leveille) ............ 332 

102. Cutaneous nerves of the shoulder and of the upper arm (after Hirschfeld and 

Leveille) 333 

103. Cutaneous nerves of the forearm and of the palm of the hand (after Hirsch- 

feld and Leveille) 333 

104. Case of right-sided serratus paralysis in a man thirty-five years of age (after 

Eichhorst) 339 

105. The same case with the arms raised ........ 340 

106. Position of the head in spasm of the splenitis capitis on the right side . . 341 

107. Musculo-spiral paralysis ........... 342 

108. Motor points of the musculo-spiral nerve and the muscles supplied by it . 345 

109. no. The distribution of the cutaneous nerves of the arm and hand (after 

Eichhorst) ............. 346 

in. Distribution of the sensory nerves on the back of the fingers (Krause) . . 347 

112. Motor points of the median nerve and the muscles supplied by it . . . 348 

113. Motor points of the ulnar nerve and the muscles supplied by it 349 

114. Motor points of the ulnar nerve ........'. 350 

115. Claw-hand (after Duchenne) 351 

116. Motor points of the musculocutaneous nerve and the muscles supplied 

by it 351 

117. Motor points of the brachial plexus ; Erb's supraclavicular point . . . 352 
118-121. The manner in which a child whose erectores spinse are paralyzed gets 

up from the ground (after Gowers) ........ 363 

122. Diagrammatic outline of the lumbar and sacral plexuses .... 364 

123, 124. Areas of distribution of the cutaneous nerves of the lower extremity 

(after Henle) 365 

125. Branches of the lumbar plexus (after Hirschfeld and Leveille) . . . 366 

126. Deep nerves of anterior and inner part of the thigh (after Hirschfeld and 

Leveille) ............. 367 

127. Cutaneous nerves of the leg and foot (after Hirschfeld and Leveille) . . 378 

128. Distribution of the branches of the external popliteal nerve (after Hirschfeld 

and Leveille) 378 



XIV LIST OF ILLUSTRATIONS. 

FIG. PAGE 

129. Motor points for the nerves and muscles of the anterior surface of the leg . 379 

130. Motor points for the sciatic nerve and the muscles supplied by it . . . 380 

131. Case of peripheral neuritis of the sciatic nerve, with shortening and atrophy 

of the affected extremity 381 

132. Case of peripheral neuritis of the sciatic nerve, with shortening and atrophy 

of the affected extremity 382 

133. 134. Contracture in the quadratus lumborum ....... 383 

I35i T 36- Panarthritis with secondary multiple neuritis 388, 389 

137. Case of myxoedema (after Charcot) ......... 399 

138. Hemiatrophia facialis ........... 402 

139,140. Cases of acromegaly (after P. Marie) 404,405 

141. Erb's juvenile muscular atrophy (after Marie and Guinon) .... 408 

142. Progressive atrophic myopathy (after Marie and Guinon) .... 410 

143. Pseudo-hypertrophy of the muscles of the legs, with atrophy of the muscles 

of the back (after Duchenne) 411 

144. Absence of the forearms 412 

145. The relations of the origin of the nerves to the bodies of the vertebras and 

the spinous processes (after Gowers) 417 

146. Scheme of the conducting paths in the spinal cord at the level of fifth dorsal 

nerve (after Flechsig) 418 

147. Cross-section through the spinal cord at different levels (after Quain) . .418 

148. Reflex arc 419 

149. Transverse section from the cervical portion of the spinal cord (after 

Charcot) 424 

150. 151. Progressive muscular atrophy (after Eichhorst) ..... 432 

152. Ascending and descending degeneration in the spinal cord (after Gowers) . 440 

153. Secondary ascending and descending degeneration in a transverse affection 

of the upper dorsal cord (after Striimpell). ...... 440 

!54) 155- Complete interruption of conduction of the spinal cord during life (after 

Eichhorst) 447 

156. Schema of the course of the nerve fibres in the spinal cord (after Brown- 

Sequard) 450 

157,158. Specimens of handwriting of patient with paralysis agitans . . 490,491 

159. Position of hands and fingers in paralysis agitans (after Eichhorst) . . . 492 

160. Position of the body in paralysis agitans ........ 493 

161. Specimen of handwriting in a case of multiple sclerosis 577 

162. Cross-section through the cervical enlargement of the spinal cord in a case of 

multiple sclerosis (after Bramwell) 583 

163. Hemiatrophy of the tongue in an otherwise perfectly healthy child . . 594 

164. Specimen of handwriting in a case of tremor in tabes 599 

165. Two cases of tabes (after Westphal) ........ 604 

166. A case of Charcot's joint in a tabetic ........ 608 

167. Erosion of the head of the humerus in tabes dorsalis (after Charcot) . .611 

168. Normal humerus (after Charcot) 61 r 

169. Skeleton of a tabetic foot (after Charcot) 612 

170. Plantar flexion of the toes in the course of tabes ...... 614 

171. Section through the cervical cord in a case of commencing tabes (after 

Striimpell) 626 

172. Section through the lumbar cord in tabes (after Striimpell) .... 626 

173. Section through the cervical cord in a case of advanced tabes (after Striim- 

pell) 626 



LIST OF ILLUSTRATIONS. 



XV 



FIG. PAGE 

174. Suspension apparatus used in the treatment of tabes ..... 636 

175. Specimen of handwriting of a patient (hat-maker) with a mercurial tremor . 666 

176. Specimen of handwriting illustrating the tremor produced in a case by the 

combined action of alcohol and mercury (V. Finkenstein, 4, 86) . . 667 

177. Specimen of handwriting illustrating alcoholic tremor 668 

178. Specimen of handwriting illustrating tremor senilis 669 



\ 



DISEASES OF THE BRAIN AND ITS MENINGES, 
INCLUDING THE CRANIAL NERVES. 



The study of brain diseases, we must confess, has not made 
the strides that might have been expected after the numerous 
and varied researches that the last decades have seen. For 
this our present very imperfect knowledge of the anatomy, and 
still more our doubts as to the physiological functions of the 
different parts of the brain must be held largely responsible. 
The structure as well as the physiological functions of the 
human brain are, up to the present time, so little understood 
that we are far from having any sure basis upon which to lay 
the foundations of a cerebral pathology. No small progress 
has been made from an anatomical standpoint through Sel- 
ling's method of serial sections, a method which Meynert, 
Henle, Wernicke, and others have not been slow to use, in 
their admirable researches, to which important additions have 
been made by the embryological studies of Flechsig, and by 
the method of " arrested development " used by Gudden and 
his pupils (atrophy method; Degenerationsmethode, Schwalbe); 
but with all this we have only here and there single stones 
which we have not as yet been able to combine for the con- 
struction of a harmonious whole. Brilliant from a physiologi- 
cal standpoint as was the discovery of Fritsch and Hitzig (1870) 
of the electrical irritability of the cortex, and of the existence 
of motor regions therein, unexpected as were the results which 
the experimental method of Munk brought to light, extraordi- 
nary and interesting as are the conclusions based upon the clini- 
cal and post-mortem observations of Charcot and his school — 
all these, wide-reaching and admirable as they were, are far 



2 DISEASES OF THE BRAIN. 

from having given us a full understanding of the functions of 
the different parts of the brain, and an explanation of the dis- 
turbances to which they are subject. Constant and untiring 
work is still needed, and the best results are promised from the 
intelligent combination of clinical observation with pathologi- 
cal research. The pathology of the brain can not be better 
advanced than by the patient clinical observation of cases dur- 
ing life and a careful autopsy after death. In institutions 
where not only the fullest opportunities are afforded for clin- 
ical observation and for the systematic conduct of post-mortem 
examinations of the brain, but where also the best men are 
found to supervise the work, in these will cerebral pathology 
make the greatest strides. 

We shall divide our description of cerebral diseases into 
three parts. In the first we shall take up the diseases of the me- 
ninges, in the second those of the cranial nerves, while the third 
will embrace the diseases of the brain in the stricter sense, i. e., 
those of the white and gray matter of the hemispheres and of 
the central ganglia. 



PART I. 
DISEASES OF THE MENINGES OF THE BRAIN. 

The meninges are relatively more frequently affected by 
disease than the brain substance itself, and quite a consider- 
able number of the cases which we commonly call diseases of 
the brain are really to be classed as affections of the meninges. 
Since these diseases can develop under the most varied con- 
ditions, and can be primary as well as secondary, they are of 
great practical importance, and we must try to distinguish 
most carefully between the different forms which they assume. 

A clear understanding of the pathological processes in these 
diseases will be facilitated by some remarks upon the anatomy 
of the meninges. 

The outermost, tough, fibro-tendinous membrane, called the dura 
mater, forms at the same time the inner periosteum of the cranial 
bones. It has an outer, rough, and an inner, smooth surface. For 
the nerves as they emerge from the skull this membrane supplies 
sheath-like coverings, among which that of the optic (vagina 
optici) is the most conspicuous. The dura consists of two layers, 
which at certain places separate, forming spaces (sinus durse matris). 
The cerebral layer sends two leaf-like processes into the cavity of 
the skull — one vertical, constituting the so-called falx cerebri (pro- 
cessus falciformis major), which extends from the crista galli to the 
internal occipital protuberance, and the so-called falx cerebelli, which 
penetrates between the two hemispheres of the cerebellum (pro- 
cessus falciformis minor) ; another horizontal, the so-called tento- 
rium cerebelli, which is pushed in between the lower surface of the 
occipital lobes of the cerebrum and the upper surface of the cere- 
bellum. Both together are called the processus cruciatus durse 
matris. The blood-supply of the dura is derived from branches of 
the meningeal arteries. That it possesses its own nerves is doubted 
by some (among them Luschka), confirmed by others (Ruedinger, 
Alexander). It is most probable, however, that it is the trigeminus 
which chiefly provides for the innervation of the dura. 



DISEASES OF THE MENINGES OF THE BRAIN. 



The second membrane, the arachnoid, is delicate and contains no 
vessels. Its outer surface is smooth and looks toward the subdural 
space, while the inner is rough and turned toward the pia mater. 
The so-called subarachnoid space, which is situated between the 
arachnoid and pia, contains between the meshes of the subarachnoid 
tissue the serous cerebro-spinal fluid. At the convexity of the brain 
the two membranes lie in close proximity, while at the base the 
arachnoid is in places raised from the pia, thus helping to form large 
spaces, the so-called cisternal subarachnoidales (Fig. i). As to the 
significance of the arachnoid villi (Pacchionian bodies) different ob- 
servers are at variance. These consist of smaller or larger bulbous 

excrescences of the 
arachnoid, are of a 
whitish color, and 
grow into the tis- 
sue of the dura, usu- 
ally in the region of 
the sinuses. Their 
function is prob- 
ably to facilitate 
the flow of the se- 
rous fluid from the 
subarachnoid space 
into the sinuses of 
the dura as soon as 
the pressure in the 
latter becomes low- 
er (Key and Ret- 
zius). 
The third membrane, the innermost, the one which lies directly 
on the surface of the brain, is called the pia mater. It dips down 
into the depths of the sulci and forms a continuous lining of those 
parts of the brain-stem which are covered by the cerebrum and cere- 
bellum, and apparently also sends processes into the interior of the. 
brain through the so-called transverse cerebral fissure. These pro- 
cesses, which are called telse choroideae, present peculiar villous 
formations, very rich in capillary vessels, and therefore of a deep-red 
color (plexus choroidei). There is a tela superior with the lateral 
choroid plexus and a tela inferior (sive cerebelli), which lies between 
the ventral surface of the cerebellum and the dorsal surface of the 
medulla oblongata. The covering or ependyma of the ventricles is 
not a part of the pia mater, but is simply a layer of epithelial cells. 
The nerves of the pia mater belong to the sympathetic. 

The diseases of the meninges of the brain consist mainly of 




Fig. 



-Cross Section through the Cerebral Cortex 
and its Membranes. 

co, Cortex ; p. pia mater ; s. a, subarachnoid space ; s. d, sub- 
dural space ; d, dura mater ; v. v, blood vessels. 



PA CH YMENINGITIS INTERNA HsEMORRHA GICA . 5 

inflammatory processes affecting either the pia or the dura 
mater. We shall study the diseases of the two membranes 
separately. 



CHAPTER I. 

INFLAMMATION OF THE INNER SURFACE OF THE DURA MATER, 
PACHYMENINGITIS INTERNA HEMORRHAGICA, HEMATOMA DURE 
MATRIS. 

The origin of the extravasations of blood which at the 
autopsy are often found on the inner surface of the dura, and 
which can be easily scraped off with the knife, is not alto- 
gether understood. Some (Virchow, 1856) hold that the pri- 
mary affection is an inflammation, and the haemorrhage takes 
place secondarily into the newly formed, highly vascular con- 
nective tissue, while others look upon the haemorrhage as pri- 
mary ; and, indeed, recent observations (Sperling) seem to be 
very much in favor of this latter view. If extensive haemor- 
rhages occur, after spreading over more or less of the inner 
surface of the dura they become encapsulated, and are then 
called hcematomata durce matris. Such a hematoma may con- 
tain from three hundred to four hundred grammes of extrava- 
sated blood, may attain the size of a man's fist, and so exert 
a deleterious pressure upon the brain. The walls are some- 
times smooth, sometimes rough ; the contents are not always 
sanguineous, but may be serous or purulent. They are most 
commonly situated at the vertex near the falx cerebri, some- 
times also in the frontal region, very rarely at the base. The 
arrangement of the haematoma in layers, which is seen on sec- 
tion, proves that the whole process consists of extravasations 
which have occurred at different times. In the least-marked 
cases only a delicate reddish membrane is found, presenting 
reddish or brownish specks, and is easily stripped off from 
the dura. Only gradually the different layers are developed, 
the one nearest to the brain, of course, being always the most 
recent, the one lying on the dura the oldest. Between the 
layers are the haemorrhages. If it happens that the most re- 
cent layer is perforated by the haemorrhage there occurs free 
extravasation of blood between the dura and the arachnoid — 
that is, an intermeningeal haemorrhage. 



6 DISEASES OF THE MENINGES OF THE BRAIN. 

^Etiology. — In the aetiology of the affection, diseases of the 
heart and kidneys, but especially chronic diseases of the brain, 
play by far the most important part. It is seen in almost all 
affections which lead to an atrophy of the brain ; further, it 
may be met with in infectious diseases — for instance, in typhoid 
fever, scarlet fever, acute rheumatism ; also in conditions of 
what we may call blood-dissolution, as in the general haemor- 
rhagic diathesis. Among the exciting causes are traumatism 
of the cranial bones and inflammation in the neighboring parts 
— for instance, in the petrous portion of the temporal bone. 
Of predominating importance, as an aetiological factor, is the 
abuse of alcohol. Almost in all autopsies on old drunkards 
we find a more or less well developed pachymeningitis interna, 
which has recently also been experimentally produced in dogs 
by continued doses of alcohol (Leyden). The fact that statis- 
tics have established that men, and more especially old men, 
are by preference affected by this disease also seems to point 
to alcohol as the principal cause. 

Symptoms may be entirely absent. This is the case if the 
haemorrhage, or the newly formed membranes were not of 
sufficient extent ; but if symptoms are present, then among the 
most important we find headache, which may persist for years, 
but which of course in itself, even if we have a history point- 
ing to this disease, as, for instance, the abuse of alcohol, is never 
sufficient to justify the diagnosis. With a sudden rise of intra- 
cranial pressure we always have apoplectiform attacks, in 
which consciousness is lost for a variable time, and in which 
the patient may die without regaining consciousness. Vomit- 
ing, slow pulse, and a very conspicuous narrowing of the pupil 
are not wont to be absent. Repeatedly peculiar dreamy con- 
ditions have been observed after such a coma, during which 
the patients seem completely dazed and the urine and fasces 
are passed involuntarily. If the haematoma lies over the mo- 
tor area, epileptiform convulsions and hemiplegia may result, 
serious motor disturbances, limited to one side, which may en- 
tirely disappear in a short while, or may last for months. Uni- 
lateral nystagmus and papillitis have been reported by some 
(Fuerstner). The further course depends upon the absorption 
of the clot or the occurrence of a further haemorrhage, as the 
case may be. The repeated development of severe cerebral 
symptoms, after striking and rapid improvement, speaks under 
certain circumstances for the existence of haematoma of the 



PA CH YMENINGITIS INTERNA HsEMORRHA GICA . 7 

dura, because it is just this frequent change in the condition of 
the patient which is characteristic of the course of the disease. 
Months and even years may thus pass without a fatal result, 
and much more rarely than one would be led to expect is it 
possible to make a positive diagnosis during life, because all 
the symptoms which we have just mentioned can be found just 
as well in other cerebral affections, in haemorrhage, embolism, 
new growths, etc., and the only thing we have to fall back upon 
is the history, if this be one of alcoholic excesses. The parox- 
ysmal appearance of new symptoms is not to be overlooked, 
inasmuch as it confirms to some extent the diagnosis of pachy- 
meningitis. However, under all circumstances the task is a 
difficult one. 

Prognosis. — The prognosis for recovery of course is abso- 
lutely bad if thickening has reached any degree worth mention- 
ing, and when we have to deal with a large haematoma which 
encroaches considerably upon the intracranial space the pros- 
pect for life is, to say the least, not hopeful. On various 
anatomical grounds death can occur suddenly and unexpect- 
edly. 

Treatment can only be of any value in the earlier stages, 
but unfortunately then the disease is usually not recognized. 
Interdiction, or at least restriction, of the use of alcohol, if this 
plays a part, energetic antiphlogistic treatment in the form of 
local bloodletting, the ice-cap to the head, counter-irritation by 
inunctions of mercurial ointment, and active purgation (calo- 
mel) would surely give us good results ; but, as we have said, 
these means are, as a rule, used too late, and as a matter of fact 
the progress of the disease is usually not altered by any thera- 
peutic measures. 

The new growths of the dura mater, as far as they at all 
manifest themselves by symptoms, will be described under the 
head of brain tumors. 



LITERATURE. 

Eulenburg, A. Lehrbuch der Nervenkrankheiten. 2. Aufl. Berlin, 1878. 

Ziegler. Lehrbuch cler allgemeinen und speciellen patholog. Anatomie. Jena, 
1882. 

Wernicke. Lehrbuch der Gehirnkrankheiten. Bd. iii, pp. 483 et seq. Berlin, 
1883. 

Gowers. Lectures on the Diagnosis of Diseases of the Brain, delivered at Uni- 
versity College Hospital, 1885. Churchhill, also Blakiston, Philadelphia. 



8 DISEASES OF THE MENINGES OF THE BRAIN. 

Liebermeister. Vorlesungen iiber die Krankheiten des Nervensystems. Pp. 306 

et seq. Leipzig : Vogel, 1 886. 
Eichhorst. Handbuch der speciellen Pathologie und Therapie. Bd. iii, pp. 439 

et seq. 3. Aufl. Wien und Leipzig, 1887. 
Striimpell. Krankheiten des Nervensystems. 4. Aufl., pp. 303 et seq. Leipzig, 

1887. 
Seeligmuller. Lehrbuch der Krankheiten des Ruckenmarks und Gehirns. Abth. 

II, pp. 401 et seq. Braunschweig, 1887. 



CHAPTER II. 

INFLAMMATIONS OF THE SOFT MEMBRANES OF THE BRAIN ; LEPTO- 
MENINGITIS f PURULENT MENINGITIS. 

A. Pathological Anatomy. ^Etiology. 

Inflammations of the soft cerebral meninges occur either 
at the base or at the convexity of the brain, according as they 
are primary or secondary — i. e., associated with other diseases 
— and one can, indeed, with a few exceptions and bearing in 
mind the transition forms, put it down as a rule that secondary, 
metastatic meningitis affects the convexity, while a primary 
meningitis is usually found at the base. 

In contradistinction to what takes place in the dura, where 
the only purulent inflammations that we find are such as have 
extended by contiguity from neighboring parts, here we have 
to deal with purulent inflammations alone. This purulent in- 
flammation of the soft membranes of the brain, the leptomenin- 
gitis cerebralis, is an infectious disease, and occurs in epidemics 
as epidemic cerebro-spinal meningitis, or more rarely sporadi- 
cally, the two forms, however, being astiologically identical. 
Besides these, we find developing in the course of tuberculosis, 
sometimes very early, sometimes late, a specific form of menin- 
gitis, the tubercular meningitis. 

Pathological Anatomy. — The pathological processes can be 
traced in the pia as well as in the substance of the brain. In 
the meshes of the former we find a purulent exudate, which is 
in rare cases limited to one hemisphere ; if it is copious, the pia 
can easily be stripped from the brain ; if it is scanty, this can 
not be done without loss of substance. The brain substance is 
cedematous and fills up the skull more than usually, so that the 
convolutions appear flattened. The ventricles are filled with 
an unusual amount of fluid (hydrocephalus internus). The 
hemorrhages which are recognizable in the brain substance do 
not exceed in size that of a pin's-head, and are either isolated 



IO DISEASES OF THE MENINGES OF THE BRAIN. 

or are seen especially near the ventricular walls in greater 
numbers, the so-called capillary apoplexies. Besides these 
there are other small punctiform haemorrhages, or rather spots 
of red softening, and minute haemorrhages closely grouped to- 
gether. All these focal changes are to be looked upon as due 
to the influence of the specific virus. If the process has be- 
come a chronic one, then the characteristic features are oedema 
of the pia, wasting of the brain substance, hydrocephalus inter- 
nus, and thickening of the ventricular ependyma, which gives 
to the surface a velvety appearance and changes the shape of 
the ventricles in a characteristic manner, the normally sharp 
edges becoming rounded off (chronic meningitis). 

In tubercular meningitis we find not only signs of an in- 
flammatory process, but also the formation of tubercles ; both, 
however, do not progress pari passu. There may be a very 
extensive eruption of tubercles and a relatively slight inflamma- 
tion, or vice versa, but always, especially in children, the greater 
part of the jelly-like exudate is situated at the base (basilar 
meningitis), between the pons and the anterior perforated 
space, and imbedded in it are the grayish-white tubercles which 
are seen as nodules, sometimes as large as millet-seeds, and are 
found in the greatest numbers among the larger vessels of the 
fissure of Sylvius, on the chiasma, pons, etc. The vessels are 
fuller than usual, and small haemorrhages can occasionally be 
seen in the pia. The substance of the brain is affected in the 
manner above mentioned — hydrocephalic effusions into the ven- 
tricles are rarely absent, and there is a decided fullness of the 
choroid plexuses. Foci of softening are noted chiefly about the 
basal ganglia ; they are produced sometimes by the occlusion of 
an artery, sometimes by the pressure which the exudate exerts 
on the vessel, or, again, by an arteritis obliterans. Regenera- 
tion has been known to occur even in tuberculous meningitis. 
Dilatation of the ventricles and other signs of an increased 
intracranial pressure may continue, and collections of fluid in 
the pia and in the ventricles may still be present, but the fluid 
may again become clear, the pia moist and non-adherent to the 
cortex, and the tubercles present no inflammation around them 
(Wernicke). 

A chronic form of basal meningitis, in which the pia is in 
places either thickened and indurated, or where we have a 
formation of brittle crusts, can be of a gummatous nature 
(Wernicke). 



LEPTOMENINGITIS. Ir 

./Etiology. — As has been stated, cerebro-spinal meningitis 
has to be looked upon as an infectious, sometimes epidemic, 
disease,, the parasitic nature of which was demonstrated by 
Leyden in 1883. He found in the tissues of the pia and in the 
turbid cerebro-spinal fluid diplococci, which A. Fraenkel rec- 
ognized as identical with the pneumococcus (Deutsche medicini- 
sche Wochenschrift, 1886, 13). Whether or not these cocci 
gain access to the meninges through the nasal cavity and the 
foramina of the ethmoidal plate, we are unable to say. Chil- 
dren and young people are more easily affected by the disease — 
which is, by the way, not contagious — than adults, and the in- 
fection can be carried by them from place to place. In inclosed 
and crowded localities, e. g., in prisons and barracks, the dis- 
ease may become endemic, a thing which Hermann (cf. lit.) has 
also observed in private houses. 

But even when there is no epidemic, the disease may ap- 
pear sporadically anywhere, and then also must be regarded as 
being just as much of a parasitic nature. 

A tangible cause for meningitis we find in traumatism of 
the cranial bones, causing injury of the soft parts, so that the 
pathogenic organisms can penetrate through the open wounds. 
The (septic ?) Streptococcus pyogenes (Eberth), which is less deli- 
cate and more resistant than the above-mentioned coccus, has 
been demonstrated in such cases. If, however, in traumatism, 
the air remains excluded, as happens in fractures at the base, 
then the presence of a purulent meningitis is difficult to ex- 
plain. 

The diseases of the bones of the skull, more especially those 
of the petrous portion of the temporal bone and of the auditory 
apparatus, play an important part in the aetiology of meningitis. 
From an otitis media may be developed a caries of the petrous 
portion of the temporal bone which may perforate the thin 
roof of the tympanic cavity. Another extension of the inflam- 
mation may come from the mastoid cells if an embolus passing 
from the veins of the bone lodges in one of the venous sinuses, 
which then becomes the seat of a purulent thrombo-phlebitis. 

That the tuberculous meningitis has its origin in tubercu- 
lous processes in other organs is clear, and the aetiology is 
therefore identical with that of tuberculosis in general — i. e., 
there is invariably an invasion of the tubercle bacillus. It is 
an interesting fact, however, that though the primary disease 
in other organs need not necessarily have produced any or at 



12 DISEASES OF THE MENINGES OF THE BRAIN. 

least no marked symptoms, we can still have secondary disease 
of the pia with the symptoms peculiar to it, which we shall de- 
scribe. Children especially are not rarely attacked by menin- 
gitis, the tuberculous nature of which is only recognized at the 
autopsy, and we may not have the faintest suspicion of the ex- 
istence of a previous tuberculous infection. In other cases, 
however, the meningitis only appears after the pulmonary tuber- 
culosis has made great progress. Caseous bronchial and mes- 
enteric glands, as well as solitary tubercles in the brain, may 
be the starting point of the meningeal affection, while it less 
commonly follows tuberculosis of the joints, bones, tubercu- 
lous affections of the intestines and genito-urinary apparatus. 

The relation of meningitis to other diseases— i. e., its simul- 
taneous appearance with pneumonia, scarlet fever, and typhoid 
fever, ulcerative endocarditis, etc. — has to be subjected to fur- 
ther study, and especially has the question to be inquired into 
whether in those cases we have to deal with a double infection 
or whether we have a single noxious agent which produces 
both the meningitis and the affection which accompanies it 
(Fel. Wolff, cf. lit.). 

It is well established that children and young people are 
more frequently and more severely attacked by meningitis than 
older persons, and it seems as if the disease is never. found in 
old age. Early childhood, the period between two and three 
years of age, furnishes relatively the greatest number of vic- 
tims and gives the most unfavorable outlook. 

B. Symptoms, Diagnosis, and Treatment. 

Symptoms. — The idiopathic, purulent meningitis of the 
adult usually begins after insignificant prodromal symptoms, 
such as digestive disturbances, hebetude, etc., with headache, 
which soon attracts by its severity and its duration the atten- 
tion of the physician. Exceptionally the patient has hours of 
comparative ease ; usually the headache is so intense that he 
becomes almost frantic. He tosses about in bed with sighs and 
groans, and, even when the mind has become dulled, involun- 
tarily again and again puts his hand to his head. Sometimes 
delirium develops early, to cease again and sooner or later 
give way to a dull and somnolent condition, which in its turn 
passes into a deep coma, the immediate forerunner of death. 

In some cases the diagnosis is facilitated by characteristic 



LEP TOMENINGITIS. 1 3 

symptoms, such as rigidity of the neck and remarkable hyper- 
esthesia of the skin and muscles. The former is especially 
well recognizable when the patient is asked to sit up in bed, 
which he can not do without intense pain ; the latter is often 
detected in the examination of the patellar reflexes, which 
themselves present no particular abnormalities. If we then 
find besides these symptoms in the beginning of the disease 
occasional (cerebral) vomiting, a strikingly slow pulse, which is 
in remarkable contrast with the elevation of temperature (102 
and more), and, what is not uncommon, marked contraction of 
the pupils, we can not easily make a mistake in the diagnosis. 
Only exceptionally, however, do we meet with a combination 
so favorable for the task of the diagnostician. More frequent- 
ly, as we shall explain at length, he has to encounter consider- 
able difficulties. There is no doubt but that the vomiting is of 
cerebral origin ; but where the center for this is to be sought, 
whether in the medulla oblongata or, as Hlasko claims (Dor- 
pat, Inaugural Dissertation, 1887), in the corpora quadrigemina, 
still remains undecided, as also does the question whether or 
not we are dealing with a functional stimulation of this center. 
Choked disks and transient paralysis of the ocular muscles are 
occasionally observed. The former is not easily recognized 
when the patient quickly passes into sopor ; the latter, how- 
ever, is recognized without difficulty by the strabismus which 
it causes and the nystagmus-like movements of the eyeballs. 
Symptoms of irritation, partly referable to the cortex, in the 
form of general or unilateral convulsions, partly to individual 
cranial nerves (grinding of the teeth, trismus, facial spasm), 
have been repeatedly noted. They seem, however, not always 
to occur, and for diagnosis must be considered as of minor 
importance. 

The course of the purulent meningitis in the adult is differ- 
ent in different cases. As a general rule, however, certain 
symptoms, especially headache and the rigidity of the neck, 
sometimes hyperassthesia of large areas of the skin, persist 
from the onset and increase, while others, as, for instance, the 
vomiting and the cranial nerve symptoms, are only transient. 

The duration of the disease can be two, three, four, to eight, 
more rarely ten to fourteen days, and the younger the patient 
the more dangerous is usually the disease. The patients die, 
as a rule, without regaining consciousness, but the coma may 
last for davs. 



14 



DISEASES OF THE MENINGES OF THE BRAIN. 



The symptoms of the epidemic cerebro-spinal meningitis 
are on the whole, as far as the brain is concerned, quite similar 
to those of the idiopathic form. In both the headache is the 
predominating symptom, and the rigidity of the neck is rarely 
absent, but in the epidemic more frequently than in the idio- 
pathic form the disease begins with a chill. The course of the 
fever presents nothing characteristic. It is sometimes of a re- 
mittent, sometimes of an intermittent type, the temperature 
sometimes reaching a height of 104 to 107 F. More or less 
severe disturbances of consciousness may occur even without 
a marked elevation of temperature. Among the cranial nerve 
symptoms, the disturbance in hearing caused by the auditory 
nerve taking part in the inflammatory process has to be men- 
tioned. Visual disturbances are more uncommon, but optic 
neuritis has been repeatedly noted. If other cerebral symp- 
toms — convulsions, hemiplegia, aphasia — occur, they have to 
be considered as complications due to an extension of the in- 
flammation to certain parts of the brain substance. 

The spinal symptoms, which are superadded, may consist 
of a distinct tenderness along the whole vertebral column, of a 
hyperesthesia of the legs (which is of diagnostic importance), 
and of twitchings of the extremities. A peculiar but, as it 
appears, extremely uncommon symptom is the so-called flexor 
contracture of Kernig : the patient when in a sitting posture 
is unable to extend his knees, because a contracture in the 
flexors is developed, which disappears as soon as the thigh is 
no longer flexed at the hip-joint. Bull (cf. lit.) has made some 
communications on this point. The mechanism of micturition 
is only influenced when the patient becomes unconscious ; then 
the urine is passed involuntarily. Besides this there are no im- 
portant bladder symptoms. The urine sometimes contains albu- 
men or sugar, also some tube-casts. Sometimes the quantity 
voided is greatly increased, a polyuria, which we have to con- 
sider as a cerebral symptom. 

Other organs rarely take part in the disease. The circula- 
tory, respiratory, and digestive apparatus usually remain nor- 
mal, and serious stomach affections, endocarditis, and pneu- 
monia, of which we have already made mention above, are 
seen only rarely as complications. Moderate splenic enlarge- 
ment often occurs. Among the skin eruptions which some- 
times accompany cerebro-spinal meningitis, besides urticaria 
and (much more rarely) roseola, we have a herpes labialis, 



LEP TOMENINGITIS. 



15 



which, without being of any prognostic value, possesses a cer- 
tain diagnostic significance. 

The course of epidemic meningitis is still more uncertain 
and variable than that of the idiopathic form. It can be rapid, 
and may end fatally within a day or a day and a half, in which 
case convulsions are followed by deep and persistent coma. It 
can, however, also be protracted and with remissions, during 
which the patient is in fairly good condition, may last for 
weeks. In the beginning of the epidemic usually grave cases 
are more common, while the longer it lasts the milder they be- 
come. It seems as if an attenuation in the virulence of the 
microorganism had taken place. There occur, besides, abortive 
cases, in which, while they undoubtedly must be classed with 
the epidemic disease, only quite a small, sometimes insignifi- 
cant, part of the symptoms are developed. The period of in- 
cubation is from three to five days. 

The symptoms of tuberculous meningitis differ somewhat in 
children and in adults. 

(a) In children the disease runs either a very acute or a 
more chronic course. In the first case only a few days may 
elapse between the onset of the trouble and the fatal issue ; in 
the latter, weeks and months may pass before amelioration 
and recovery, or in these cases also death takes place. 

The acute form usually begins suddenly with epileptiform 
convulsions. Apparently healthy, robust children fall into 
convulsions and then complain of severe headache and nausea, 
which is often followed by vomiting ; the pulse becomes irregu- 
lar, and its variations in frequency are more striking than in 
any other disease. On examination, we find the temperature 
only moderately elevated, but the patient is very restless, 
throwing himself about in bed and complaining of pain in the 
abdomen, chest, etc. Strabismus, trismus, grinding of the 
teeth, are often noted, and on mechanical stimulation of the 
skin striking circumscribed red spots, Trousseau's tdches cere- 
brates, appear. The patients sigh deeply when examined, or 
give an unexpected loud, sharp cry, the cri hydrocfyhalique, a 
very unfavorable symptom which is of far greater importance 
than the spots, from the appearance of which we are not justi- 
fied in drawing either favorable or unfavorable conclusions. 
The approach of death is announced by an enormous increase 
in the frequency of the pulse, by renewed convulsions, and 
deep coma. 



l6 DISEASES OF THE MENINGES OF THE BRAIN. 

The chronic form begins insidiously and gradually, the 
first thing to attract our attention being the change in the 
disposition of the child. Previously gay, friendly, playful, and 
companionable, he becomes peevish, irritable, unmanageable, 
and willful. On the least provocation he begins to cry and to 
be naughty, so that the parents find it necessary to punish 
him. It is not until the sleep begins to be disturbed and the 
child tosses about all night and groans in its sleep, wakes up in 
the morning without having rested, and complains of headache 
that the parents become apprehensive, and the loss of appetite, 
the occasional vomiting, the obstinate constipation, and the pale, 
sickly appearance confirm the fear that a serious malady is on 
the point of showing itself. The symptoms may for weeks re- 
main obscure ; high temperature may alternate with low, a fre- 
quent with a slow pulse, without it being possible to say any- 
thing definite about the case. Only when one day an epilepti- 
form attack occurs, the headache increases in intensity, the 
child becomes somnolent, cries out during sleep, shrinks on 
being touched (hypergesthesia of the skin), only then is the con- 
dition clearer, and finally can not be mistaken when such a 
focal symptom as paralysis of the eye muscles appears. Even 
then remissions may occur, and decided, though in most cases 
only temporary, improvement is not excluded. The outlook 
is always doubtful, and can, even when the prospects appear 
most favorable, be very serious. 

(b) In adults the difference between the chronic and acute 
form is less marked than in children. Patients who have by 
no means presented definite signs of tuberculosis begin to com- 
plain of vague headache, general prostration and malaise ; their 
sleep becomes disturbed and restless ; especially in the morn- 
ing they feel tired and unstrung ; they complain of loss of ap- 
petite, and may have occasional vomiting spells. In some cases 
the psychical symptoms are the most prominent, and it may 
happen that the disease begins with the symptoms of a delirium 
tremens, especially if the patient be a drinker. In all cases the 
sensorium becomes sooner or later dull ; the patient appears 
dazed, gives confused answers, and conveys in general the im- 
pression of a man whose mind is affected. Not rarely delirium 
comes on ; in it the excitement and exaltation are the most 
prominent features. But with all these symptoms the influence 
of a severe, agonizing headache still makes itself known, and 
even during unconsciousness the patients often raise the hand 



LEP TOMENINGITIS. j y 

toward the head, throw themselves about in bed restlessly 
with groans, and seem sensitive to the slightest touch or tap 
on the head. The participation of certain cranial nerves, es- 
pecially the oculo-motor and the abducens, is evident from the 
transient ptosis, the inequality of the pupils, and the strabis- 
mus ; the ophthalmoscopic examination not uncommonly re- 
veals choked disks. If in looking for the latter we are able to 
find tubercles in the choroid, this is of course of the highest 
importance for the diagnosis. The facial nerve, which often 
becomes affected, may be the seat of spasm or of paresis. If 
we remember that the base of the brain is the chief seat of the 
inflammation we can easily understand why these cranial 
nerves should be implicated. If motor disturbances, consist- 
ing of general or unilateral convulsions, or of hemiplegia or 
paresis, as well as speech disturbances, make their appearance, 
we may assume that an eruption of tubercles has occurred in 
the brain cortex. The more pronounced these disturbances, 
which are to be regarded as focal symptoms, the more likely 
is it that circumscribed tuberculous softenings exist in the 
cortex. Sometimes also a peculiar tonic rigidity develops in 
all four extremities which seems to be of reflex origin. The 
reflexes, at first increased, but presenting nothing character- 
istic, usually lose in intensity as the disease goes on, and finally 
disappear altogether. With regard to the sensory changes, it 
should be remarked that hyperassthesia of the skin is not as 
regular a symptom in this as in the first described form of 
meningitis. The temperature, as a rule, is somewhat above 
the normal, yet it varies, and occasional remissions may be 
followed by elevations, or it may remain constantly between 
ioi° and io2° F., or thereabouts. Nothing certain, however, 
can be said about it. Strumpell reports a temperature of 88° 
during the agony. Equally variable is the pulse, which as a 
rule is slowed. We may count 40 to 50 beats a minute, while 
in a few hours it may rise to 100 or 120. 

Other organs take but a small share in the disease, and even 
the lungs show signs only when simultaneously affected with 
miliary tuberculosis. If the respiration assumes a Cheyne- 
Stokes type (after a series of shallow respirations, which be- 
come deeper and deeper, a complete pause), this is usually a 
bad omen. 

To say anything positive about the course of tuberculous 
meningitis is impossible. It is not constant, but sometimes 
2 



!8 DISEASES OF THE MENINGES OF THE BRAIN. 

acute, sometimes chronic, sometimes presenting long inter- 
missions, and sometimes steadily progressive. A subdivision 
into different stages may look very well on paper, but to dem- 
onstrate them at the bedside is only rarely possible. A 
period of cerebral irritation has been distinguished from one 
of increased intracranial pressure, and this again from a period 
of paralysis. The first has been thought to be characterized 
by headache, vomiting, and delirium ; the second by slowing 
of the pulse and paralyses ; the third, finally, by increase in the 
frequency of the pulse, elevation of temperature, and deep 
coma. But such a division entails no practical benefit, as the 
so-called " stages" are often not distinguishable from each 
other, but pass directly one into the other. From the instruct- 
ive treatise of Hirschberg (cf. lit.) we learn that even the man- 
ner of onset may vary much, and that it may be difficult, even 
in the stage of focal symptoms, to make a diagnosis. If a con- 
sumptive suddenly develops symptoms of motor or sensory 
paralysis or irritation, this should always make us suspect the 
existence of a tuberculous process in the brain. 

Diagnosis. — None of these different forms of meningitis that 
we have described is easy to diagnosticate, with the excep- 
tion, perhaps, of the epidemic cerebro-spinal. When several 
cases have occurred in a community the recognition of new 
ones presents no difficulty, especially if we keep in mind the 
frequency with which herpes labialis is met with in the disease. 

Of all diseases, perhaps typhoid fever is most likely to be 
mistaken for meningitis. There is no doubt, and it has been 
shown by reliable observers (Curschmann), that there are cases 
in which meningitic symptoms are very well marked, but in 
which typhoid bacilli are found in the cord at the autopsy to 
be the infectious agent. We might be led to believe that at 
least the characteristic temperature curve, the splenic enlarge- 
ment, the condition of the stools, and the rose spots would be 
sufficient to make a mistake impossible, but this is by no means 
always the case; there are instances in which typhoid fever 
can not with certainty be excluded, and then the differential 
diagnosis is simply impossible. 

If uraemia enters into the question of diagnosis, the exam- 
ination of the urine (for tube-casts, etc.), suppression of the 
urine, if it should be present, and the appearance of the con- 
vulsions will facilitate the recognition of the true condition. 

Whether we have to do with a case of croupous pneumonia 



LEP TOMENINGITIS. 



I 9 



or with meningitis is, in the majority of cases, easy enough to 
decide. Both affections may, however, occur together, and 
then it is important to remember that marked hyperesthesia of 
the skin, staggering gait, and rigidity of the neck all may be 
present with pneumonia alone. If this be complicated by 
oedema of the glottis, so that respiration is difficult, the patient 
will fix his head in order to bring into play the auxiliary mus- 
cles of respiration, and thus in the recumbent position too the 
rigidity of the neck is simulated (Wernicke). The existence of 
meningitis is only, then, to be assumed if pronounced basal 
symptoms are present, especially if paralysis of the eye mus- 
cles has existed for a certain period of time. 

More frequently delirium tremens is associated with men- 
ingitis, and we are not always able to decide whether the deli- 
rium, the tremor, and the epileptiform convulsions are refer- 
able to the latter or to the former. 

According to Reynaud (cf. lit.) there are cases in which, al- 
though the symptoms of tuberculous meningitis seem pro- 
nounced, in a few weeks the patient completely recovers, in 
which instances the assumption that there is a pseudo-men- 
ingitis of hysterical origin seems necessary. Of course, the 
previous history of the patient, the family history, etc., have to 
be taken into consideration before such a diagnosis, which we 
think is always very risky, can be even thought of. 

The occurrence of meningitic symptoms as a consequence of 
worms, which Devaux (cf. lit.) has upheld, is certainly excep- 
tional, and can hardly, for any length of time, give rise to an 
error in diagnosis. 

With sufficient care we can easily avoid confounding men- 
ingitis with eclampsia infantum. 

Prognosis. — -The prognosis in every case of meningitis is 
very serious ; we are never in a position to predict with any 
certainty the outcome, not even when everything seems to be 
going on very favorably, and grave symptoms have not de- 
clared themselves. These may suddenly develop in one night, 
and a patient whom we have left in fairly good condition in 
the evening may the following morning be hopelessly ill. On 
the other hand, we should not give up our patient too soon ; the 
gravest symptoms may fade away, and improvement is still 
possible even where the case seems desperate. Undoubtedly, 
however, meningitis is one of the most serious diseases, and 
one in which recovery is rare, the epidemic cerebro-spinal 



20 DISEASES OF THE MENINGES OF THE BRAIN. 

meningitis being- the only form which runs occasionally a more 
favorable course. 

Partial recoveries are much more frequently seen than ab- 
solute ones; if, for example, in the course of meningitis, a 
hemorrhagic inflammation of the inner ear develops, this gives 
rise to permanent deafness, which in younger children, as a 
rule, leads to deaf-mutism ; or if purulent inflammation of the 
eyeball, a panophthalmitis or a choroiditis coexist with the 
meningitis, this may entail a grave disturbance of sight, even 
phthisis bulbi, and complete amaurosis. In either of these 
cases the meningitis may get well, but in one deafness, in the 
other impairment or loss of sight, and in the most unfavorable 
cases both remain behind without the development of any 
mental defects. Blindness may also be a consequence of an 
optic neuritis, which does not get well, but causes shrinking of 
the optic nerve and atrophy of the disk. Cases of meningitis 
confined to the convexity sometimes recover, leaving a more 
or less marked feeble-mindedness. 

Treatment. — The treatment is first to be directed against 
the inflammation, and later endeavors should be made to aid 
absorption of exudates if such be present. The former is to 
be combated by local bleeding and the application of cold, also 
by inunctions of mercurial ointment, four to eight grammes ( 3 j 
to 3 ij) a day to the shaved head. In some cases we shall suc- 
ceed with such measures in lessening the severity of the symp- 
toms, but often little or nothing is achieved by them. Painting 
the shaved head with tincture of iodine is objectionable, owing 
to the disagreeable and painful tension which it produces, and 
which is but little alleviated by ice. That free purgation with 
large doses of calomel actually produces an antiphlogistic 
effect can not be proved, but there is no reason why it should 
not be tried, the drug being given until the characteristic 
stools appear. The absorption of exudates is attempted by 
large doses of potassium iodide, 4 to 6 grammes (3 j to 3 jss) a 
dav in hot milk, a medication which is especially indicated in 
the gummatous form of meningitis. 

During coma the patient may be put into a tepid bath 
(go to 93 F.) and cold water (66° to 6o° F.) be poured over 
his head. These cold-water affusions may be continued for 
eight or ten minutes, with the result, frequently, of actually 
rousing the patient out of his unconsciousness, an improve- 
ment, however, which generally does not last very long. The 



LEPTOMENINGITIS. 21 

repetition of this procedure several times a day is therefore 
necessary, notwithstanding the considerable difficulties with 
which it is (at least in private practice) attended. 

Symptomatically the agonizing headache and the jactita- 
tions may be met with morphine. The same drug is used 
against the obstinate vomiting, which is hard to treat, and in- 
deed may resist all efforts. It may happen that all internal 
medicines, cracked ice, champagne, opium, aromatic tinctures, 
etc., as w r ell as all applications of spiritus sinapis, etc., remain 
without effect ; then we are forced to resort to morphine, the 
subcutaneous administration of which generally accomplishes 
more than all remedies previously used. The regulation of the 
bowels should of course never be overlooked. 

We can only, then, reasonably hope for success from our 
therapeutic efforts if we pay careful attention to the nutrition 
of the patient. As soon as this is left out of sight the battle 
is practically lost in spite of all medicines and inunctions. 
More than in any other disease it is here the chief task of the 
physician to see that the strength of his patient is kept up, so 
that he be fit if necessary to stand an illness of weeks, and 
more than in any other disease is here the prolonged use of 
wine indicated, and is much more important than all drugs. 
Besides wine, a tablespoonful of beef-tea is to be given every 
hour. This is prepared by gradually heating lean beef, cut into 
small cubes, after the addition of a little salt, in a lightly 
closed glass bottle over the water-bath, and cooking it until 
the pieces are completely disintegrated. Two pounds of meat 
furnish about a cupful of beef-tea. 

In very Exceptional cases operative measures are indicated, 
namely, where we have sufficient reason to suspect the exist- 
ence of an exudation in the ventricles, which would manifest 
itself by an aggravation of the symptoms of increased intra- 
cranial pressure. Trephining may then be resorted to if the 
circumstances are in other respects favorable. 

The treatment of tuberculous meningitis in children has to 
be conducted according to the plans just laid down, with this 
difference — that the inunctions of the head with mercurial oint- 
ment are to be replaced by the administration of calomel, 
three to five centigrammes (grs. ss. to j) every two hours. 
Besides, the inunctions of the head with iodoform ointment, 
lately so warmly recommended, should be tried; but here, too, 
the preservation of the strength must be our chief aim. Milk, 



22 DISEASES OF THE MENINGES OF THE BRAIN. 

with the addition of a little Hungarian wine or a few drops of 
cognac, should always be kept ready. 

LITERATURE. 

Gottwald. Meningitis tuberculosa. Diss, inaug. Breslau, 1870. 
Seitz. Die Meningitis tubercul. cler Erwachsenen. Berlin, 1874. 
Striimpell. Zur Pathologie und pathol. Anatomie der epidemischen Cerebro- 

spinalmeningitis. Deutsches Arch. f. klin. Med. 
Chantemesse. Etude sur la meningite tubercul. de l'adulte. These de Paris, 

1884. 
Leichtenstern. Ueber epidemische Meningitis. Deutsche med. Wochenschr., 

31, 1885. 
Bull. Ueber die Kernig'sche Flexionscontractur der Kniegelenke bei Gehirn- 

krankheiten. Berl. kl. Wochenschr., 47, 1885. 
Reynaud. Arch, de Neurol, xiv, 42, p. 409, 1887. 

Schultze. Verhandl. des VI. Congresses fur innere Med. Wiesbaden, 1887. 
Hirschberg. Abnorme Form der Meningitis tuberculosa. Deutsches Arch. f. 

klin. Med. Bd. 41, Heft 6, 1887. 
Leyden. Bemerkungen iiber Cerebrospinalmeningitis und iiber das Erbrechen 

in fieberhaften Krankheiten. Zeitschr. f. klin. Med., xii, 4, 1887. 
Lardier. Meningite a frigore, effet remarquable du tannin. Rambervillers, 1887. 
Herrmann. Breslauer arztl. Zeitschr. 16, 1887. 
Richter. Ibid., n, 14, 1887. 
Devaux. Oxyures et symptomes pseudo-meningitiques. Progr. m6d., No. 46, 

1887. 
J. Simon. Diagnostic differentiel de la meningite tuberculeuse. Gaz. des 

Hop., No. 132. Nov. 1887. 
Ferret. Progres med., xv, 41, 1887. 
Wolff, Felix. Bemerkungen iiber das Verhalten der Cerebrospinalmeningitis zu 

den Infectionskrankheiten. Deutsche med. Wochenschr., 50, p. 1080, 1887. 
Weichselbaum. Ueber die Aetiologie der acuten Mening. cerebro-spin. Fort- 

schr. d. Med., 18, 19, 1887. (" Diplococcus intercellularis meningitidis.") 
Hofmann v. Ueber die acute Meningitis in angeblich ursachlichem Zusammen- 

hange mit Misshandlungen oder leichten Verletzungen. Wiener med. Woch- 
enschr., 6, 188S. 



PART II. 

DISEASES OF THE CRANIAL NERVES. 

If we once have a clear idea that in the cranial nerves we 
have to distinguish the origin, which in all probability is found 
in the cortex and the nuclear region of the medulla oblongata, 
from the partly central (intracerebral), partly peripheral (ex- 
tracerebral) course, it is self-evident that the diseases of the 
cranial nerves are divisible into those which affect the nerve at 
its origin, the center, and those which affect it in its course. As 
we shall come to deal in the next part of our book with the 
affections of the brain substance proper, it necessarily results 
that in the following chapters we must either touch upon 
things which properly belong to Part III, or that in the latter 
we shall not be able to avoid some repetition. Neither of these 
courses is without objections ; still, from a practical point of 
view, we have deemed it best to treat of the diseases of the 
cranial nerves here in toto. 

The central lesions of the cranial nerves often form merely 
a part of a more general disease of the nervous system. Those 
of peripheral origin occur also independently — for instance, as 
the result of exposure to cold, traumatism, etc. In very many 
cases we are not able to determine definitely whether the dis- 
ease has a central or a peripheral origin. For a clear under- 
standing of the following chapters, a knowledge of the anatomy 
of the parts naturally can not be dispensed with. Some remarks 
bearing on this, which, of course, are not meant to take the 
place of a detailed study, have therefore been inserted at the 
head of each chapter to recall to the reader's mind in outline 
the necessary anatomical relations. 



2 4 



DISEASES OF THE CRANIAL NERVES. 



CHAPTER I. 

DISEASES OF THE OLFACTORY NERVE. 

The olfactory nerve begins in a small pyramidal lobule, the tu- 
ber olfactorium (caruncula mamillaris), the base of which is situated 
in front of the anterior perforated space. At its beginning, the nerve 




Fig. 2. — Anterior and Middle Portions of the Base of the Brain. F., frontal 
lobe. T., temporal lobe. b. o/., olfactory bulb. tr. o/., olfactory tract, t. o/., tuber 
(trigonum) olfactorium. s.fn., middle, s. /., lateral root. ?'., infundibulum (cut off). 
cm., corpora albicantia. I. p. a., anterior perforated space, s.p.p., posterior per- 
forated space. 

is broad, but narrows into a band somewhat prismoidal on section, 
which is called the olfactory tract, and which in its turn ends in an 
oval gray swelling, the olfactory bulb {vide Fig. 2). From the lower 
aspect of this bulb, which lies on the cribriform plate of the ethmoid 
bone, two groups of fibers pass through the little openings of the 
bone into the nasal cavity, and it is only the sum of these filaments 



DISEA SES OF THE OLFA CTOR Y NER VE. 2 5 

(the fila olfactoria) which can be looked upon as the nerve of smell 
in the strict sense of the term. The olfactory tract and bulb are 
parts of a cerebral lobe, the so-called olfactory lobe. 

The origin and the course of the roots of the olfactory nerve (the 
strise olfactorii, Schwalbe) are not known. It is, however, generally 
agreed that there are three roots. The outermost, the strongest, is 
said to be traceable into the island of Reil. Schwalbe supposed the 
existence of a lateral root (radix lateralis, seu longa, seu externa) 
originating in the hippocampal convolution, and of a median (radix 
medialis, seu interna, seu brevis), coming from the gyrus fornicatus. 
Others have looked upon the anterior commissure and the corpus 
striatum as the starting points of the olfactory nerve, but nothing 
positive is known. An olfactory center has been assumed in the 
gyrus hippocampi and in the gyrus uncinatus. Lately Zuckerkandl 
has claimed that the cornu Ammonis is a part of the olfactory 
center. 

Notwithstanding the fact that the affections of this nerve 
are not of very great practical importance, they afford a great 
deal of interest, because they may under certain circumstances 
(i. e., if a careful clinical description is followed by an exact 
and accurate post-mortem account) give us some information 
about the anatomical and physiological questions concerning 
the course and origin of the nerve, and again because they 
may attain a considerable importance and value in the diag- 
nosis of certain cerebral diseases. 

The olfactory nerve may be diseased in its central or in its 
peripheral portion. In the former case it may be the olfactory 
center which is affected, or the conduction may be interfered 
with somewhere in the course of the intracerebral paths. 

Since, as we have stated, the situation of the olfactory cen- 
ter is not definitely known, we can not be expected to know 
much about its diseases. It would appear, however, that it may 
be affected by destructive as well as by irritative lesions ; the 
latter manifest themselves by hallucinations, the former by loss 
of smell (anosmia). Among the diseases in which hallucina- 
tions of smell occur are various psychoses, also migraine, tic 
douloureux, epilepsy, and tabes. Usually the smell which such 
patients describe is bad, disgusting — of faeces, sometimes of 
poisonous plants, putrid substances, etc. (kakosmia) — and it is 
rare for them to imagine that they smell pleasant substances. 
One of my cases, who, owing to an ocular paralysis, was treated 
with the galvanic current passed through his head from one 



2 6 DISEASES OF THE CRANIAL NERVES. 

side to the other, declared that he smelled oil of lavender from 
the moment the current was closed until it was again broken. 
This seems to point to the possibility that by the galvanic cur- 
rent the olfactory center may be stimulated. Central anosmia 
is sometimes observed in cerebral lesions which cause hemi- 
plegia and aphasia, the disturbance being confined to the nos- 
tril on the same side as the lesion. Anosmia is also known to 
occur in hysteria and in old age ; in the latter case it is proba- 
bly to be attributed to atrophy (senile anosmia). Cases have 
been repeatedly noted in which tumors of the anterior fossa of 
the skull, exostoses, meningitis at the base of the frontal lobe, 
have given rise to anosmia. 

Interference of conduction in the olfactory nerve may be 
assumed in cases where there is a history of traumatism — a fall 
upon the head, more especially upon the occiput. According 
to Carbonieri, complete loss of smell suggests strongly disease 
of the olfactory tract or bulb. 

The treatment in the central affections of the olfactory nerve 
must of course be directed against the underlying disease. 

Of greater practical interest are the peripheral affections of 
the olfactory, which chiefly consist in a decrease of the power 
of smell. Leaving out of consideration the common cases in 
which an acute or chronic nasal catarrh causes partial or even 
temporarily complete anosmia, the sense of smell may be 
affected as the result of abnormal dryness of the nasal cavity 
(diminution in the secretion of tears in trigeminal anaesthesia, 
diminished flow of tears into the nasal cavities in facial paral- 
ysis). Not rarely certain occupations give rise to anosmia, 
which is sometimes associated with a tolerance of disagreeable 
odors which at first were highly obnoxious to the workers. 
Such anosmias are to be found in soap-boilers, catgut spinners, 
tanners, skinners, and butchers, whose sense of smell is often 
considerably dulled ; again it may be due to disturbances in 
nutrition, to the action of caustic substances, or injury to the 
peripheral nerve endings — effects which are due to the chemi- 
cal composition of the inhaled substances. Thus we have ob- 
served loss of the sense of smell in those working in chlorinated 
lime, while it was found to be diminished in working men occu- 
pied with the pulverization of chromeironstone. Strieker has 
also known it to occur in an entomologist in consequence of 
the protracted inhalation of ether. 

The treatment consists in faradization (Beard and Rockwell) 



DISEASES OF THE OLFACTORY NERVE. 



2? 



and galvanization (Fieber) of the nasal cavity, or painting with 
a one-per-cent solution of strychnine (in olive oil). The use of 
irritative snuff powders has repeatedly been recommended for 
anosmia of peripheral origin, but has frequently been used 
without benefit. Spontaneous recovery is not rare. Finally, 
we may say a word or two about the method of testing the 
sense of smell. All those substances which irritate the trigem- 
inus should be avoided, as, for instance, acetic acid, smell- 
ing salts, snuff, tobacco ; the patient would feel what he can 
not smell, and we might be thus led astray in our conclusions. 
Cologne water, oil of rosemary, musk, camphor, anise, oil of 
turpentine, asafcetida, sulphureted hydrogen, are sufficient for 
most tests. That each nasal cavity must be tested separately 
goes without saying. 

LITERATURE. 

Notta. Recherches sur la perte de l'odorat. Arch, gener. de med., April, 1870. 
Ogle. Anosmia, or Cases illustrating the Physiology and Pathology of the Sense 

of Smell. Med.-chir. Transact., 1870, liii. 
Molliere. Note pour servir a 1'histoire du nerf olfactif. Lyon med., 1871, No. 20. 
Carbonieri. Zur Localisation des Centrum olfactorium. Riv. clin., xxiv, 9, p. 

657. September, 1885. 
Erben. Wien. med. Blatter, 1886, No. 43, 44 (kakosmia in tabes). 
Moldenhauer. Die Krankheiten der Nasenhohlen u. s. w. Leipzig, Vogel, 1886. 
Gowers. Lectures on the Diagnosis of the Diseases of the Brain, delivered at 

University College Hospital, London. Churchill, 1885. Also Blakiston, 

Philadelphia, 1885. 
Thudichum. On the Nature and Treatment of Hypertrophies and Tumors of the 

Nasal and Pharyngeal Cavities. The Lancet, August 27, 1887, p. 401. 
Zuckerkandl. Ueber das Riechcentrum. Stuttgart, Enke, 1887. 
Roth. Die Erkrankungen der Nasenschleimhaut, ihre Beziehungen zum iibrigen 

Organismus und Behandlung derselben. Centralbl. fur d. ges. Therapie, v, 

Heft x, October, 1887. 



CHAPTER II. 



DISEASES OF THE OPTIC NERVE. 



The optic nerves derive their fibers from the occipital lobes, the 
optic thalami, the outer and inner geniculate bodies, the anterior 
corpora quadrigemina, and the cerebellum (through the superior 
peduncle of the cerebellum). 

What are known as the optic tracts before the chiasm is reached, 
after this point become the optic nerves. These are round hard cords, 
about four millimetres in diameter, which, passing in a diverging 
direction through the optic foramina, enter the orbits and reach the 
eyeballs after their passage through the orbital fat. Here they pass 
the sclerotic and choroid and spread themselves over the fibrous 

layer of the retina. The outer 
covering of the nerve, which is 
a process of the dura mater, is 
called the durai sheath; the 
process of the pia, the inner 
or pial sheath. The two are 
separated by a space which be- 
longs to the lymphatic system, 
the so-called intervaginal or 
subvaginal space. The arteria 
centralis retinae, a branch of 
the internal carotid, enters the 
optic nerve about fifteen or 
twenty millimetres from the 
eyeball and runs together with 
the vein of the same name in 
the substance of the nerve to the retina. 

The chiasm, which is formed by the union of the optic tracts, is a 
flattened four-sided body, in which the crossing of the optic fibers 
takes place. This crossing, as we now know with a fair amount 
of certainty, is, however, only partial, a semidecussation. The fibers 
from the outer half of the retina (represented by an interrupted line) 
pass to the center without decussating, while those of the inner half 




Tract. 



Fig. 3. — Diagram showing the Course of 
the Optic Fibres in the Chiasm. 



DISEASES OE THE OPTIC NERVE. 29 

cross over and pass to the centre of the opposite side (cf. Fig. 3). 
Each occipital lobe, therefore, receives fibres coming from the tem- 
poral as well as from the nasal half of the retina. Thus, for in- 
stance, the left receives fibres from the outer temporal half of the 
left and from the inner nasal half of the right retina. In diseases of 
this lobe, therefore, images falling upon the left half of the retina, 
or, in other words, those which lie in the right half of the field of 
vision, are no longer perceived — right-sided hemianopia. 

The optic tract, the superficial fibres of which can be traced into 
the white covering of the pulvinar (the so-called stratum zonale thai- 
ami), originates by two roots — an outer, much stouter, the end ganglia 
of which are the anterior corpus quadngeminum, the outer genicu- 
late body, and the pulvinar, and by an inner root which can be 
easily followed to the inner geniculate body (Wernicke). These end 
ganglia of the optic tracts form at the same time the terminal points 
of certain fibres of the corona radiata, which run in a sagittal direc- 
tion forward from the occipital lobe, and are connected with the 
pulvinar, the brachium anterius of the quadrigeminal body, and the 
outer geniculate body. This bundle of fibres is the sagittal medul- 
lary tract of the occipital lobe, or what is called the optic radiation, 
and is designated in the diagram by s (vide Fig. 4). 

The exact localization of the cortical centre of vision has not as 
yet been established. According to Ferrier, it is in the angular 
gyrus; according to Munk, it is in the convex surface of the occip- 
ital lobe. 

It would be beyond the scope of the present work to treat 
in extenso of those diseases of the optic nerve which belong 
strictly to the domain of ophthalmology ; they can be con- 
sidered here only as far as they are connected with the nervous 
system. To these belong, first of all, certain inflammatory con- 
ditions which act upon the intraocular end of the nerve, the 
papilla (disk), and give rise to what we therefore term papil- 
litis (choked disk). The name optic neuritis, which is fre- 
quently used as a synonym for papillitis, is inexact, because it 
may imply an affection of the whole nerve trunk. 

The papillitis, choked disk (Staimngspapille , as the Germans 
call it, after von Graefe, 1859), i s frequently, although not al- 
ways, met with in cases of intracranial tumors, and is (accord- 
ing to von Graefe) to be attributed to a high grade of venous 
engorgement, produced by an impediment to the reflux of the 
venous blood into the skull cavity. Later, when Schwalbe had 
discovered that there was a communication between the fluid 



3Q 



DISEASES OF THE CRANIAL NERVES. 



contents of the skull and the intervaginal space of the optic 
nerve, it was shown that the subdural space was distended 
with a serous inflammatory fluid, and that the optic nerve at its 
passage through the lamina cribrosa of the sclerotic becomes 
compressed (Schmidt-Rimpler). Finally, Deutschmann (cf. lit.) 




J 



Fig. 4.— Diagram showing the Origin of the Optic Nerve. (After Wernicke.) 
/>, crusta of the cms cerebri ; sn, substantia nigra ; cgi, inner, cge, outer geniculate 
body; qp, brach. post. corp. quadr.; qa, brach. ant. corp. quad.; pu, pulvinar ; s, optic 
radiation. 

has put forth the view that papillitis is not caused by mechan- 
ical influences, but that it is due to the action of pathogenic 



correct further experience will show. Besides the pure papil- 
litis there is also found a papillo-retinitis, the ophthalmoscopic 
picture of which differs from that of the former affection, and 
which is to be referred to a meningitis, which has advanced 
along the sheath of the optic nerve. 

A pure papillitis, as we have said, is chiefly found in intra- 
cranial tumors. Patients in whom a brain tumor is suspected 
ought to be examined for choked disks even if they do not 
complain of any subjective symptoms pointing to it, because 
sight may, even if the disk is markedly swollen, remain normal 
for a long time. Only when the nerve or the chiasm is strongly 
compressed does amblyopia or amaurosis occur in the early 
stages. 



DISEASES OF THE OPTIC NERVE. 



3* 



The seat of the tumor has nothing to do with the occur- 
rence of papillitis. Basal neoplasms can, through direct press- 
ure upon the optic nerve, cause a simple atrophy of the same. 
Nor does the nature of the tumor play any part here. Gum- 
mata, tubercles, entozoa (cysticerci, echinococci), carcinomata, 
gliomata — any one of these may produce a papillitis, which is 
usually bilateral (in ninety-three per cent of the cases, Annuske 
and Reich), although the processes need not necessarily be 
equally developed in both eyes. 

Of practical importance are the sudden spells of blindness 
which occur sometimes in the course of a papillitis, termed by 
H. Jackson epileptiform amaurosis. They are probably due 
to a temporary swelling of certain tumors and the consequent 
compression of certain areas of the brain or the vessels (Leber) 
distributed to them. These attacks may last for hours or days, 
and either disappear completely or leave a permanent increase 
in the amblyopia. The ophthalmoscopic examination does not 
teach us anything about this periodical blindness. 

A papillitis rarely ever gets well ; in by far the greater 
number of cases a papillitic atrophy and total amaurosis takes 
place, first in one and then in the other eye. Cases in which 
one eye is seriously damaged while the other remains per- 
fectly well are extremely rare. I have, however, had occasion 
to observe an instance of this with Magnus. More frequently 
both eyes become diseased, one soon after the other. Dropsy 
of the ventricles may give rise to a simultaneous amaurosis of 
both eyes. 

Papillo-retinitis is not very rare in tubercular basilar men- 
ingitis ; in epidemic cerebro-spinal meningitis it is exceptional. 
Chronic cerebral affections of children often lead to it, the 
amaurosis in these instances usually developing quickly, while 
the general symptoms become intensified. 

Inflammations of the optic-nerve trunk occurring alone may 
be caused by cold, febrile diseases, disturbances in menstrua- 
tion, and hereditary influences. On ophthalmoscopic examina- 
tion either nothing remarkable or only a slight blurring of the 
disk is recognizable, because the inflammation affects more 
especially that part of the nerve which is behind the eyeball 
(retrobulbar neuritis of von Graefe). The disturbance of vision 
usually begins gradually, and is confined either to the periphery 
of the field of vision or it consists of a central amblyopia or a 
circumscribed central amaurosis. It does not terminate in com- 



32 DISEASES OF THE CRANIAL NERVES. 

plete blindness ; frequently only marked disturbance of color 
vision remains. 

To the neurologist the cases of optic neuritis in patients 
with a neuropathic family history are of extreme interest. 
Such persons usually suffer even in early youth from migraine, 
nervous palpitation of the heart, vertigo, sometimes also from 
epileptiform attacks. Between the ages of twenty and thirty 
they begin to complain of trouble with their sight, either of 
subjective light or color sensations or else that objects appear 
to them enveloped in a dense mist ; within from four to six 
weeks they may become completely blind, but their blindness 
as a rule does not persist, but gives place to a central ambly- 
opia with normal sight at the periphery of the field of vision. 
The prognosis differs markedly in different families. It is of 
interest to note that as a rule only the male members of the 
family are wont to be affected by the disease. 

In the second place we will consider atrophy of the optic 
nerve. It consists in a wasting of the nerve elements, and may 
be either primary (genuine) or inflammatory, the consequence 
of a previous neuritis. It may also affect the trunk of the 
nerve as well as the intraocular end of it. If the nerve, besides 
the wasting of its pulp, also undergoes a diminution in its 
volume, so that it appears like a gelatinous grayish-yellow cord, 
the atrophy is known as gray degeneration. 

Tumors and inflammatory exudates, as well as splinters of 
bone, may by pressure, by shutting off the blood supply (as, 
for instance, in embolism of the arteria centralis retinae), and 
through interference with the nutrition lead to atrophy. 

The progressive atrophy, or, as it is better termed, progress- 
ive gray degeneration, which may be of cerebral or spinal 
origin, is characterized clinically by a diminution in the acute- 
ness of the central vision, a contraction of the whole visual 
field, and disturbance of the color sense. In the ophthalmo- 
scopic examination the bluish-white discoloration of the disk 
and the atrophic excavation of the nerve (due to wasting of the 
substance of the disk) are very apparent. The acuteness of 
vision, grows gradually but progressively less, and months and 
years may pass before complete amaurosis is developed. On 
the other hand, the whole process may run its course in two or 
three weeks. The contraction of the field of vision is rarely 
concentric ; usually the defects are in one direction only, and are 
often sectorial (Leber). Enormous contraction of both fields of 



DISEASES OF THE OPTIC NERVE. 



33 



vision, with at the same time normal acuteness of sight in the 
center, which was eventually followed by blindness, has been 
observed by Schweigger. The disturbance in color vision is at 
first limited to the perception of green, which is confused with 
white or gray, the perception of blue and yellow being rela- 
tively longest retained. The atrophy develops bilaterally, 
although one eye alone may at first be affected, and the other 
eye remain intact for years. 

Foci of softening in the brain, progressive paralysis of the 
insane, sometimes also epilepsy, are the cerebral diseases in 
which the affection is not rarely observed. It is besides also 
noted in multiple sclerosis, although in this disease it never 
leads to total amaurosis, a fact which Charcot is in the habit of 
emphasizing in his lectures. 

More important is the fact that in locomotor ataxia optic 
atrophy is comparatively frequent. Wharton Jones (British 
Medical Journal, July 24, 1869) makes the sympathetic respon- 
sible for this, assuming that the paralysis of the vaso-motor 
nerves, producing first hyperasmia, leads finally to atrophy of 
the optic nerve. This explanation, however, is at once over- 
thrown by the fact that in the optic atrophy of tabes there are 
at no time any traces of hypersemia. We shall again have to 
refer to this question in our account of tabes, where we shall 
also consider the treatment of optic atrophy. 

Congenital optic atrophy can sometimes be traced to hered- 
itary influences, or to consanguinity of the parents ; sometimes 
it is due to hydrocephalus. Injury to the skull in consequence 
of instrumental interference at birth very rarely has anything 
to do with it. 

The diseases of the chiasm and optic tract may be consid- 
ered together, since they possess one symptom in common 
which is of special interest to the neurologist — viz., hemianopia. 
This symptom is also found associated with diseases of the 
centre of the optic nerve in the occipital lobe. It is the only 
form of visual disturbance where one can with certainty diag- 
nosticate a central affection of the optic nerve. It is likely to 
be of cortical origin if the hemianopia occurs suddenly as the 
only symptom, there being no change to be found on ophthal- 
moscopic examination ; whereas if other symptoms accompany 
it — aphasia, hemiplegia, etc. — this idea of a cortical lesion must 
be given up. By hemianopia in general we mean a loss of one 
half (the right or the left) of the field of vision, so that patients 
3 



34 



DISEASES OF THE CRANIAL NERVES. 



affected with right-sided hemianopia see only the objects which 
are in the left half of their visual field, whereas those to the 
right are not perceived. If the disturbance affects the halves 
on the same side of both eyes — that is, the nasal on the one, the 
temporal on the other — we call it a homonymous hemianopia. 
If in both fields the temporal halves are lost, this constitutes 
what is known as temporal hemianopia, which is of rarer occur- 
rence ; the absence of both nasal halves of the field of vision 
does not seem to occur, and the superior and inferior hemian- 
opia, where the line of division is not vertical but horizontal, 
seems to be extremely rare. 

The explanation of the hemianopia in lesions of the cortical 
center for sight is quite evident if we accept, as is now gener- 
ally done, the existence of the above-described semidecussa- 
tion of the fibres in the chiasm. The path from the optic tract 
to the cortex of the occipital lobe may be divided into the fol- 
lowing segments (Wernicke) : The first includes the optic radia- 
tion in the occipital lobe, the lesions of which give rise to 
homonymous hemianopia without any other focal symptoms ; 
the second will include the place where the fibres of the optic ra- 
diation enter the internal capsule, and the ganglia of origin of the 
optic tract, the pulvinar, and the outer geniculate body — hemi- 
anopia and hemianassthesia ; the third will include the optic 
tract in its course at the base of the brain — hemianopia with 
hemiplegia. If in the region of the visual centre or the optic 
radiation a bilateral focal lesion occurs, then we may have 
complete blindness setting in with an apoplectiform attack. 
This is in reality a bilateral hemianopia (Wernicke). Of diag- 
nostic value in these cases is sometimes the so-called hemian- 
opic pupillary reaction (Heddaeus, Wernicke), although it is 
not absolutely reliable. With the mirror of the ophthalmo- 
scope we reflect the light first upon the left, then upon the 
right half of the retina, and observe the pupillary reaction. 
If the reflex occurs normally, the optic tract must be intact, 
and the disturbance must be due to a bilateral lesion of the 
optic radiation in the occipital lobe, or in the cortical center. 
If the reflex is not obtained we must assume a lesion of the 
optic tract of the corresponding side. Light perception and 
pupillary reflex go in this case hand in hand. 

In diseases of the chiasm hemianopia has been repeatedly met 
with, but in this case we have not a homonymous, but a bitem- 
poral hemianopia, as in the case of Oppenheim, where gumma- 



DISEASES OF THE OPTIC NERVE. 



35 



tous disease of the chiasm was responsible for the disturbance 
(cf. Virch. Arch., 1886, Bd. civ, 2, p. 306). Quite lately the same 
author has described an " oscillating " bitemporal hemianopia 
in diseases of the chiasm, which he considers as pathognomonic 
of basal cerebral syphilis (cf. lit.). 

If the tissue injured by the lesion which has caused the 
hemianopia is capable of regeneration, as may be the case where 
we have a haemorrhage or an inflammation, the defect will 
pass off completely, whereas if this is not the case the trouble 
remains stationary, without, however, any additional disturb- 
ance of sight. Such a condition, which often develops as the 
consequence of an apoplexy, may persist for years, but no 
second attack, by which the centres of the other tract also may 
be disturbed, is to be feared, as such a thing has never been 
observed. 

The examination in a case of hemianopia may (roughly) be 
conducted in the following manner : The patient is to be placed 
at a distance of about two feet from the examiner, and, if the 
right eye is to be examined, asked to cover his left eye with his 
hand, while with the right eye he fixes the left of the examiner 




Left and Right Eye. (After Fo'rster.) 



who covers his right eye. The examiner then holds up his 
finger between the patient and himself, and moves it in different 
directions as far as the border of his own field of vision, the pa- 
tient at the same time being: asked how far out he is able to see 



36 DISEASES OF THE CRANIAL NERVES. 

the finger. The examiner is thus enabled to notice every mo- 
tion of the patient's eye toward the object, and, judging from his 
answers, can compare the patient's field of vision with his own. 
Instead of the finger a small piece of white paper fastened on 




Fig-. 6. — Field of Vision of the Left and Right Eve in Lkft-sided Hemiano- 
tia. (After Gowers.) 

a dark penholder may be used in a similar way. These tests 
should be made in a good light (Donders, Gowers). 

The more extensive defects can always be found out by this 
method ; for slight ones a perimetric examination is indispen- 
sable. An accurate determination of the field of vision with 
the help of the perimeter can only be attained by practice. A 
description of the instrument and its use is here not necessary. 
Figs. 5 and 6 illustrate (i) the normal fields of the left and right 
side ; (2) the fields in a case of left-sided hemianopia. 

The so-called flitting scotoma (amaurosis partialis fugax, or 
temporary hemianopia) has in all probability also to be regarded 
as an affection of the centre for vision. The disturbance comes 
on in paroxysms. At first a dark spot appears in the field of 
both eyes, which increases in a crescentic or horseshoe form. 
It begins to scintillate and becomes bounded by a bright zig- 
zag line of brilliant colors. If this has after fifteen or twenty 
minutes reached the border of the field of vision, it disappears 
from the centre toward the periphery and the field clears up 
again. Most probably in all cases the affection is bilateral. 
The attacks, which last from a half to three quarters of an 
hour, occur with variable frequency, sometimes only once dur- 
ing the whole life, and it is interesting to note that they are al- 
most always associated with attacks of migraine. Of the causes 



DISEASES OF THE OPTIC NERVE. 



37 



nothing is known, although the belief that hard mental work- 
ers are especially prone to it is not without foundation ; but 
there are numerous cases in which we are reduced to regard 
sexual and alcoholic excesses, cold, etc., as astiological factors. 
As we are not acquainted with any remedies for the disease, 
we have to be satisfied in prescribing tonics and strengthen- 
ing diet, quinine, and, above all, mental as well as bodily rest. 

The nature and the seat of those forms of amblyopia which 
develop under the influence of certain toxic substances are still 
obscure. Material changes in the retina are usually absent, 
and only quite late may a slight or partial discoloration of the 
papilla become visible. 

To this class of substances belong more especially alcohol, 
tobacco, and lead. 

The alcoholic amblyopia is the most frequent form. In, the 
mildest cases it manifests itself as a simple central amblyopia 
without distinct scotomata, without disturbances in color vision, 
and without contraction of the visual field ; whereas in the most 
serious forms, which may occur after excessive indulgence in 
spirits, especially in persons of previously moderate habits, 
there may be an acute, almost total blindness. After the recur- 
rence of such attacks a more severe form of atrophic disease of 
the optic nerve may develop, with which is associated discol- 
oration of the whole disk. Central colored scotomata and sim- 
ple scotomata, disturbances in color sense in the whole visual 
field, are then not rare. The ophthalmoscopic examination 
does not reveal anything very characteristic. Vision rarely 
becomes less than -J^ to ^ ¥ , and complete recovery even in the 
most marked cases is possible. The few examinations of the 
optic nerve which have been made after death seem to indicate 
that alcohol exerts a direct injurious action upon the nerve it- 
self. The latter has several times been found in a state of fatty 
degeneration with or without compound granular corpuscles 
and thickening of the interstitial tissue which contains the ves- 
sels (Erismann, Leber, cf. lit.). Since it has recently also been 
shown that alcohol can act in a similar way upon the peripheral 
nerves this pathological condition is more easily understood. 

Similar in its development and in its course is the so-called 
tobacco amblyopia, which, ceteris paribus, is, however, more 
rarely met with than the alcoholic form, and is more benign, 
inasmuch as it usually passes off after the cause is removed. 
The diagnosis is, as a rule, easy enough, as other signs of 



3* 



DISEASES OF THE CRANIAL NERVES. 



chronic nicotine poisoning (digestive disturbances, palpitation 
of the heart, insomnia) are rarely wanting. The disease seems 
only to occur among those who use tobacco in some form or 
other, in smokers or chewers, while the workers in tobacco, 
who are exposed to the inhalations of the tobacco dust and of 
a certain amount of nicotine, seem, so far as experience goes, 
not liable to the complaint. 

The one form of amblyopia which has been more carefully 
studied than any other, but which nevertheless is not much 
better known or understood than the affections which we have 
just treated of, is lead amblyopia (amblyopia saturnina), in 
which the field of vision may remain normal or in which there 
may have developed central scotomata or contraction of the 
visual field. Pronounced neuritis, with decided swelling of 
the disk and with peripapillary haemorrhages, has been ob- 
served, and the termination in complete amaurosis is not rare. 

Under certain still unknown conditions a sudden bilateral 
blindness may develop without previous decrease of vision — 
amaurosis saturnina. It is commonly preceded by lead colic. 
The affection, which bears a certain resemblance to the amau- 
rosis of uraemia, may sometimes improve with remarkable 
readiness after the removal of the injurious cause. 

In a given case we should, for the sake of confirming our 
diagnosis, never fail to search for other cerebral symptoms 
common to chronic lead poisoning, such as epileptiform attacks, 
hemiplegia, speech disturbances, and so forth. 

About the relative frequency of the disease no definite 
statement is possible, nor do we know which particular occu- 
pation in the lead industry is the most dangerous, or after 
how long an exposure eye trouble develops in lead workers. 
The role which the so-called individual predisposition plays in 
this connection seems as important as it is obscure. 

In the treatment of the alcoholic amblyopia, local bleeding 
with Heurteloup's cups, active purgation, diaphoretics, and 
later strychnine injections are of service. In tobacco ambly- 
opia the treatment is the same, but bleeding may be dispensed 
with. In the saturnine form purgatives are indicated, also 
opium and subcutaneous injections of morphine. In all cases, 
however, the prompt and permanent removal of the injurious 
agent is a sine qua non ; where this can not be done the out- 
look for recovery is always very doubtful. 

Besides the substances mentioned, quinine and mercury 



DISEASES OF THE OPTIC NERVE. 



39 



may lead to disturbances of sight, which in their course resem- 
ble those just described. 

LITERATURE. 

Tanquerel des Planches. Traite des maladies de plomb ou saturnines. Paris, 

1839, t. ii, pp. 208-225. 
Hirschler. Amaurosis saturn. Wien. med. Wochenschr., Nos. 7 and 8. 1866. 
Haase. Amaurosis saturn. geheilt durch subcutane Morphiuminjection. Ze- 

hender's M. Bl.V, pp. 225-228. 1867. 
Cyon. Die Lehre von der Tabes dorsalis. Berlin, 1867. 
Erismann. Ueber Intoxications-Amblyopien. Zurich. Diss, inaug. 1867. 
Leber. Graefe's Archiv. Bd. xv, 3, pp. 60 et seq. 1869. 
Forster. Ueber den schadl. Einfluss des Tabakrauchens auf das Sehvermogen. 

Jahresber. d. schles. Gesellsch. fur 1868. 
Samelsohn. Zur Casuistik der Amblyopia saturn. Zehender's M. Bl. xi, pp. 

246-250. 1873. 
Hutchinson. Report on the Prognosis in Tobacco Amaurosis. Ophthalm. 

Hosp. Rep., viii, 3. 1876. 
Graefe-Saemisch. Handbuch der gesammten Augenheilkunde. Bd. v, Theil v. 
Leber. Die Krankheiten des Sehnerven, pp. 757 et seq. Leipzig, 1877. 
Reich. Zur Statistik der Neuritis optica bei intracraniellen Tumoren. Klin. 

Monatsschr. f. Augenheilk., xii. Stuttgatt, 1874. 
Forster. Beziehungen der Allgemeinleiden u. Organerkrankungen zu Veran- 

derungen u. Krankheiten des Sehorgans. Leipzig, Engelmann, 1877. 
Plobin. Des troubles oculaires dans les maladies de l'encephale. Paris, Bail- 
Here, 1880. 
Magnus. Die Blindheit, ihre Entstehung und Verhiitung. Breslau, Kern, 1883. 
Grossmann. Zur Diagnostik der Augenkrankheiten mit Bezug auf Localisation 

von Cerebrospinalleiden. Wiener Klinik, x. Heft, Oct., 1884. 
Schoeler und Uhthoff. Beitrage zur Pathologie des Sehnerven und der Netz- 

haut bei Allgemeinerkrankungen. Berlin, Peters, 1884. 
Jacobson. Beziehungen der Veranderungen u. Krankheiten des Sehorgans zu 

Allgemeinleiden u. Organ-Erkrankungen. Leipzig, Engelmann, 1885. 
Peltesohn. Ursachen u. Verlauf der Sehnervenatrophie. Centralbl. f. prakt. 

Augenheilk., pp. 45, 75, 106. 1886. 
Bergmeister. Die Intoxicationsamblyopien. Wien, 1886. 
Gowers, loc. cit., p. 87. 1886. 
Michel. Ueber Sehnervendegeneration und Sehnervenkreuzung. Wiesbaden, 

1887 (Festschrift). 
Nettleship. Lancet, July 16, 1887 (Quinine Amblyopia). 
Uhthoff. Untersuchungen iiber den Einfluss des chronischen Alkoholismus 

auf das menschl. Sehorgan. V. Graefe's Arch., Bd. xxxiii, Abthl. 1. 
Oppenheim. Die oscillirende Hemiopia bitemporalis als Kriterium der basalen 

Hirnsyphilis. Berl. klin. Wochenschr., No. 36, 1887. 
Deutschmann. Ueber Neuritis optica, bes. die sogen. Stauungspapille. Jena, 

Fischer, 1887. 
Siemerling. Ein Fall von gummoser Erkrankung der Hirnbasis mit Betheiligung 

des Chiasma. Arch. f. Psych., xix, 2, pp. 401 et seq. 1888. 



CHAPTER III. 

DISEASES OF THE NERVES SUPPLYING THE OCULAR MUSCLES 1. E., 

THE THIRD (MOTOR OCULl), THE FOURTH (p ATHETICUS), AND 
THE SIXTH (ABDUCENS). 



The third nerve emerges from the brain at the inner margin of 
the crus close to the anterior border of the pons; it passes obliquely 
forward and outward, reaches the outer wall of the cavernous sinus, 
enters it, and then divides into two branches, which, passing through 

the sphenoidal fissure 
qua 



enter the orbit. The 
upper division, which 
supplies the levator 
palpebral superioris 
and the rectus supe- 
rior, is the smaller of 
the two. Of the three 
branches of the lower 
division, the one sup- 
plying the inferior ob- 
lique is the longest; 
the two others, one of 
which goes to the in- 
ferior rectus, the oth- 
er to the internal rec- 
tus, are shorter. The 
7.— Cross Section through the Region of the , , , . . 

ant. Corpora Quadrigemina. longest branch, that 

qu. a. anterior corpora quadrigemina ; g.c. gray matter around ° e mrenor OD- 

the aqueduct of Sylvius; aq, aqueduct of Sylvius; nlll lique, gives off a 
nucleus of the third nerve ; ///. posterior longitudinal bun- gftort TOOt to the cili- 
dle ; r. k. red nucleus (tegmentum) ; sn, substantia nigra , . , - . 

(locus niger) ; p, cerebral peduncle. ai 7 ganglion, the fila- 

ments of which are 
distributed to the ciliary muscle (tensor choroideae) and to the con- 
strictor of the iris (sphincter pupillae); consequently these intrinsic mus- 
cles of the eyes are also innervated by the third nerve, while the dila- 
tor pupillae, on the other hand, is provided for by the sympathetic. 




DISEASES OE THE MOTOR NERVES OF THE EYE. 



41 



The nuclei of the third nerve, a column of multipolar ganglionic 
cells, lie above the posterior longitudinal bundle, between it and the 
aqueduct of Sylvius, and the root fibres coming from them divide 
into several fasciculi, pierce the posterior longitudinal bundle, the 
tegmentum, with the red nucleus and the substantia nigra, and 
emerge from the brain at the place shown above (cf. Fig. 7). 

Experimental as well as clinical observations seem to indicate 
that in the collection of ganglionic cells of this nerve nucleus there 
exist three centres, the anterior of which is the centre for the ciliary 
muscle (accommodation) ; the next the centre for reflex stimulation 
of the iris by light ; the third, by far the largest, the centre for the 
extrinsic ocular muscles (Gowers). Observers, however, by no 
means agree with regard to the number and position of the indi- 
vidual oculo-motor nuclei or centres. The view held by Gowers is 
diagrammatically illustrated in Fig. 8. 

That there exists a cortical centre for the ocular muscles and the 
levator palpebrarum is beyond question ; nothing certain is, however, 
known about its situa- „ 

tion ; most probably it 
lies in the upper or low- 
er parietal lobe (cf. Ex- 
ner, Untersuchungen 
iiber die Localisation 
der Functionen in der 
Grosshirnrinde des 

Menschen. Wien, Brau- 
mtiller, 1881, p. 42). 

The fourth, the 
trochlear or pathetic 
nerve, is the smallest of 
the cranial nerves, but 

has the longest course within the skull cavity, 
brain close behind the corpora quadrigemina at 
face of the valve of Vieussens ; from here it 
and downward course, winds around the outer 




fig. 8.— dlagramatic longitudinal section through 
the Pons with the Nuclei of the Ocular nerves. 
(After Gowers.) C. Q. Corpora quadrigemina ; a a' bb' 
and c c represent the centres and the nerve-fibres ; a, for 
accommodation, b, for the reflex activity of the iris, c, 
for the extrinsic ocular muscles ; all three are contained in 
the oculomotorius. IV, pathetic. VI, abducens. 



leaves the 



It 
the upper sur- 
takes a lateral 
side of the crus 

cerebri, and reaches the base of the brain. Its course is now forward ; 
piercing the dura mater behind the anterior clinoid process, it reaches 
a small channel of the cavernous sinus, and runs alongside of the 
third to the sphenoidal fissure, pierces its fibrous membrane, and 
finally enters the superior oblique muscle. 

The nucleus of the fourth lies behind the collection of cells 
from which emanates the third nerve (Wernicke), to the ventral side 
of the aqueduct of Sylvius, on the posterior longitudinal bundle, in 
the gray matter around the aqueduct. From this nucleus the root 



42 



DISEASES OF THE CRANIAL NERVES. 



originates, which, passing to the mesial side of the descending root 
of the fifth (Fig. 9, Vd), extends as a round bundle (IV) to the pos- 
terior corpus quadrigeminum ; in the substance of the valve of Vieus- 
sens it is crossed by the nerve of the opposite side, and emerges 
finally in the above-described manner on the side opposite to that in 
which its nucleus is situated. 

The sixth nerve, the abducens, leaves the brain at the poste- 
rior margin of the pons, between it and the anterior pyramid. It 




Fig. 9. — Cross-section through the Region of the Tegmentum. (After Schwalbe.) 
d, patheticus-crossing. IV, Patheticus at its exit. IV cross-section of the patheticus in 
its course to the nucleus. V.d. descending root of the trigeminus (cross-section) ; aq, 
aqueduct, g. c, central gray substance around the aqueduct, s./, substantia ferrugin. d, 
sup. peduncle of cerebellum crossing at c ; r, raphe ; f.r, formatio reticularis , h.l. pos- 
terior longitudinal bundle. 



takes at once a forward course and passes into the cavernous sinus, 
piercing its posterior wall ; it then runs, surrounded by the dural 
sheath, alongside of the internal carotid, and, emerging through the 
sphenoidal fissure, enters the external rectus, in the substance of 
which it breaks up into branches. 

The nucleus of the abducens, which was at one time thought to 
be connected with the root of the facial nerve (hence the facial- 
abducens nucleus of Meynert and Stilling), lies in the floor of the 
fourth ventricle, from which it is separated by the ependyma. The 
abducens root, passing through the peduncular portion of the pons 
to the outer side of the pyramids into the tegmental regien of the 
pons to the median side of the upper olive, enters finally this nucleus 
(cf. Fig. 10). The tegmentum behind the lemniscus is divided into 
three parts by the abducens (and facial) root, the inner two of which 
Meynert has called the motor region of the pons. 



DISEASES OE THE MOTOR NERVES OE THE EYE, 



43 



The affections of the nerves supplying the ocular muscles 
belong, strictly speaking, also to the domain of ophthalmology. 
Since, however, they are of such importance for the diagnosis 
and the prognosis in certain nervous diseases, it is necessary 
to devote a few pages at least to the description of their symp- 
toms and the proper methods of examination. 

The independent diseases of the muscles of the eyes may 
be of a paralytic or of an irritative (spastic) nature, the latter 



9lTI 



YILa YUa 




Fig. 10. — Cross-section through the Pons. (After Schwalbe.) n VI, abducens nu- 
cleus. VI, abducens. O.S., upper olive. aV, ascending root of trigeminus. nVII, 
nucleus of facial, n VIII, auditory nucleus (so-called external nucleus). VII, emerging 
portion of facial root, po, transverse fibres of the pons which are divided into superficial 
po 1 and deep po' 2 . py, pyramidal tract. 



class, however, being by far the less frequent of the two. Their 
seat may be central or peripheral, although we should state 
that an undoubted central affection of the abducens and of the 
patheticus has never been observed. Of oculo-motor paralysis, 
we are acquainted with a peripheral and a central form. 

A peripheral affection may have its seat in the stem or in 
its branches ; a central, in the nucleus or the (supposed) cortical 
center of the nerve. The former will be characterized by the 
absence of all cerebral symptoms, which, in the central form, 
are almost always present. It can be brought about by patho- 
logical changes in the orbit, in which case the eyeball not 
infrequently protrudes and becomes immobile. Further, it 
may develop as a rheumatic paralysis from exposure to cold 



44 



DISEASES OF THE CRANIAL NERVES. 



{a frigore), also in constitutional syphilis, diphtheria, and in 
other acute infectious diseases ; exceptionally it is seen after 
traumatism. In one of my cases a man was kicked by a cow- 
in his right eye ; after the acute symptoms had passed off, a 
paralysis of the levator palpebral superioris remained for 
months. Power of vision was not interfered with. 

The central paralysis is met with in the course of menin- 
gitis, multiple sclerosis, progressive bulbar paralysis, and, 
above all, locomotor ataxia. It affects but rarely all the ocular 
muscles at the same time, but either the extrinsic or intrinsic 
alone. It has, moreover, been seen after poisoning with fish 
(Alexander, Bresl. arztl. Zeitschr., 3, 1888). Although the 
diplopia of the tabetics is neither a constant nor a pathogno- 
monic symptom of the disease, the occurrence of transient 
double vision in otherwise apparently healthy persons ought 
always to make us suspicious, and ought to induce us to sub- 
ject the patient to a more careful examination. The nature as 
well as the anatomical seat of this oculo-motor paralysis occur- 
ring in tabes is entirely obscure. 

Of the cortical oculo-motor paralysis we know little or 
nothing ; the only well-established fact is that an isolated 
paralysis of the levator palpebras superioris may be associated 
with cerebral affections — for instance, with a cerebral haemor- 
rhage and a consequent hemiplegia. The reason of this may 
possibly be that the levator is the only muscle supplied by 
ocular nerves which can be voluntarily moved on one side 
only (Mobius) ; were this only possible in conjunction with the 
other, the paralysis would not occur. This " blepharoptosis 
cerebralis " needs much further investigation. 

In very exceptional instances in otherwise healthy individu- 
als there occurs a paralysis of the eye muscles, which, defying 
all treatment, may persist for years without the appearance, 
however, of any other symptoms, whether cerebral or spinal. 
I have the notes of several cases of this nature ; since, how- 
ever, none ol them came to autopsy, I shall abstain from any 
detailed report. 

In studying the symptoms of the paralyses of the ocular 
muscles we shall first consider those of the oculo-motor pa- 
ralysis, more especially of the complete form, in which all 
branches of this nerve are implicated. 

The upper eyelid droops completely, and the eye can only 
be opened slightly by the aid of the frontalis ; the movements 



DISEASES OF THE MOTOR NERVES OF THE EYE. 45 

of the eyeball are also at fault ; the eye, deviated outward as 
it is, can not be moved toward the nose ; similarly any up- 
ward motion is impossible, as such depends upon the supe- 
rior rectus and the inferior oblique. On the other hand, the 
outward movements are unhampered (rectus externus), while 
the downward motion is performed by the superior oblique, 
the pure action of which can here be well studied, the rectus 
inferior, which otherwise also assists in the downward motion 
of the bulb, being now inactive. 

From the different directions of the axes of the two eyes 
there results a very apparent symptom — namely, strabismus — 
which may be convergent or divergent, according to the mus- 
cles -affected. This strabismus, due to paralysis of the ocular 
muscles (paralytic), differs from that caused by spasm (spas- 
modic), inasmuch as (1) in the latter the deviation exists with 
all movements, while in the former only with those which call 
into action the paralyzed muscle ; (2) in spasmodic strabismus 
the secondary deviation of the sound eye, of which we shall 
presently speak (cf. p. 47), does not occur. 

The double vision, " diplopia," which is associated with 
strabismus, is especially marked at the beginning of the dis- 
turbance, before the patient has learned to suppress the " false 
image " seen with the affected eye, and only to pay attention 
to the " true image " seen with the healthy one. At first these 
double images cause him much annoyance until later on he 
learns to close the affected eye by contraction of the orbicu- 
laris, or to put the head into a position in which the affected 
muscle is not called into play. By these devices he not only 
avoids the unpleasantness of the double images, but also the 
consequences which the erroneous projection of the visual 
field entails, namely, a peculiarly disagreeable feeling of dizzi- 
ness, the so-called ocular or visual vertigo, to which we shall 
have occasion to refer again. 

With reference to the pupillary symptoms we must keep in 
mind the reactions present in a normal eye: the pupil reacts 
directly to changes between light and darkness, contracting if 
light is thrown into the eye, and indirectly by sympathy, in 
that the pupil of one eye dilates if the other is covered ; it also 
reacts on motions of convergence and on forced accommoda- 
tion, contracting in either case. All these reactions are lost in 
complete paralysis of the third nerve. The pupil is moder- 
ately dilated and gives no response to the influence of light or 



46 DISEASES OF THE CRANIAL NERVES, 

accommodation ; if the paralysis is incomplete, and either the 
sphincter of the iris or the ciliary muscle or both are intact, so 
that in the latter case only the extrinsic muscles do not perform 
their function, the size of the pupil can vary and accommoda- 
tion be retained. 

The reflex immobility of the pupil (Erb), also called the 
"Argyll-Robertson pupil " — that is, where the pupil has lost 
its reaction to light impressions (reflex), but has retained its 
power of accommodation — is very frequently observed in 
tabetics. Besides this, the pupil in tabes is often very small, 
pin-head-pupil — spinal myosis. 

Paralysis of the abducens, unilateral or bilateral, which also 
comparatively frequently accompanies locomotor ataxia, often 
constituting here the only initial symptom for a long time, is to 
be recognized by noticing that the eye, which is slightly turned 
inward, can not be moved outward, while all the other move- 
ments are unimpeded. In exceptional cases this is found asso- 
ciated with facial paralysis. A case of this sort, in which the 
paralysis was congenital, has lately been reported by Mobius 
(cf. lit.). 

Unilateral paralysis of the patheticus, which supplies the 
superior oblique muscle, is always difficult to recognize even 
when the muscular system of the other eye remains perfect, and 
can only be diagnosticated after an examination of the nature 
of the double images. When there is paralysis of the oculo- 
motorius in the other eye a diagnosis is impossible. The ex- 
amination ought to be made by an ophthalmologist in order to 
establish the absence of power in the superior oblique. Ex- 
tremely rare is the bilateral patheticus paresis, which has been 
noted in some cases of tumor of the pineal gland. The ana- 
tomical conditions directly underlying it are not known (Re- 
mak, cf. lit.). 

A paralysis of the patheticus, superadded to a paralysis of 
the oculomotorius, may be recognized by the absence of the 
characteristic rotation around the sagittal axis, which would 
otherwise occur on looking down (Wernicke). 

If several muscles of one eye which are supplied by differ- 
ent nerves are paralyzed, or if there exist paralysis of the mus- 
cles of both eyes, we speak of an ophthalmoplegia (Hirschberg, 
Mauthner), and we distinguish an external ophthalmoplegia if 
only the extrinsic, and an internal ophthalmoplegia if only the 
intrinsic muscles of the eye are paralyzed (sphincter, dilator, cil- 



DISEASES OF THE MOTOR NERVES OF THE EYE. 



47 



iary muscle). The so-called ophthalmoplegia progressiva (von 
Graefe) will be described in the eleventh chapter of this part 
under the name of poliencephalitis superior (Wernicke). Quite 
lately our attention has been drawn to a so-called recurrent pa- 
ralysis of the third nerve, of which Mauthner has analyzed four- 
teen instances. This disease is characterized by the fact that 
only one, and always the same, oculo-motor becomes affected, 
and that the paralysis is always complete — that is, takes in all 
the branches. Females seem more predisposed to the affec- 
tion than males. The duration of the individual attacks varies 
from one, three, four, to even six months. They may recur 
after an interval of from four weeks to a year. Other nervous 
symptoms — migraine, vertigo — may or may not accompany 
them. The attacks may recur during the whole life of the 
patient, and even in the intervals traces of paralysis may re- 
main (Mobius, Remak). Whether there are instances in which 
the disturbance is only functional, or whether in all cases there 
exists a distinct organic basis, we are with our present mate- 
rial unable to decide definitely, and we are equally in the dark 
with reference to the seat of the affection, as to whether it is of 
peripheral or of central origin. That there are instances where 
the former is true is proved by a case published by Richter (cf. 
lit.), where a new growth in the nerve itself was found. 

In a suspected paralysis of the ocular muscles we endeavor to 
make out in our examination any defects in the mobility of the 
eyeball. For this purpose the patient is asked to follow with his 
eyes the finger of the examiner in different directions without 
moving his head. In this way every asymmetry in the move- 
ments of the two eyes can be noted. If the mobility in the direc- 
tion of the action of the affected muscle is defective (" primary 
deviation "), nystagmus-like twitching is sometimes observed 
on attempts at extreme rotation in that direction. But it 
may happen that the paresis of a muscle is not recognized if its 
innervation is particularly strong ; then we have in the corre- 
sponding muscle of the other eye so abnormal an innervation 
that in the latter the effect is excessive and we get a so-called 
" secondary deviation " of the sound eye. This can easily be 
demonstrated if the presumably healthy eye is first covered 
with the hand and the patient endeavors to fix with the paretic 
e}^e a point which it can not reach at all or only with the ut- 
most exertion. If, then, the fixing eye is covered, we observe 
whether the healthy eye be in a proper position or not, and 



4 8 



DISEASES OF THE CRANIAL NERVES. 



shall find that the latter has been moved too far in the desired 
direction. If this method does not give any satisfactory re- 
sults, we have to examine into the nature of the double images. 
One eye of the patient having been covered with a colored 
glass, he is asked to follow with his eyes (of course, again with- 
out moving his head) the flame of a candle which is moved to 
and fro. If there exists paralysis or paresis in one eye, the 
patient complains of seeing two flames, which become the far- 
ther apart the more the affected muscle is exerted. But if now, 
for instance, the patient looking toward the left complains of 
diplopia, this may be due to paralysis of the left external or the 
right internal rectus, as both of these muscles move the eyeball 
to the left. To determine which of these two is not perform- 
ing its function properly, we must ascertain from the patient 
whether the double images are homonymous or crossed — that 
is, whether the colored picture be on the same or on the oppo- 
site side to the eye covered with the colored glass (homony- 
mous and crossed diplopia respectively). In the former case 
the abducens (rect ext.) is the nerve affected ; in the latter the 
oculomotorius (rect. intern.). For a minute study of the double 
images, the reader is referred to the plates and the work of 
Landolt, of Paris, which has been translated into German by 
Magnus (cf. lit.). 

The associated lateral movements of the eye to the right 
and to the left may be interfered with in the following ways: 

i. There may exist a so-called conjugate deviation of the 
eyes — that is, a permanent fixation of both eyeballs to one side, 
which can only be overcome, and then but temporarily, by the 
strongest effort. We shall refer to this symptom again in our 
account of hemiplegia. 

2. Motion of both eyes toward one side may be permanent- 
ly lost. In this case we have a paralysis of the abducens of the 
one and paralysis of the internal rectus of the other side, and 
the eyes are turned not toward the affected, but toward the op- 
posite side. In such cases the lesion is situated in the lateral 
portion of the pons, near the abductor nucleus. If the centres 
of both sides which lie close together are paralyzed, the eyes 
which are fixed in the middle can be moved neither to the 
right nor to the left, but only upward and downward, the up- 
per eyelid moving normally (Wernicke). 

3. The upward and downward motion of the eyes may be 
lost and only the lateral motion be possible. This form of the 



DISEASES OF THE MOTOR NERVES OF THE EYE. 49 

associated ocular palsy, in which also both upper lids may be 
paralyzed, is caused by a lesion of the centres situated in the 
central gray matter of the third ventricle and the aqueduct of 
Sylvius — that is, in the region of the oculo-motor nucleus. If 
this be accompanied by a hemiplegia, we are justified in diag- 
nosticating a lesion of the pyramidal tract at the level of the 
upper corpus quadrigeminum, the posterior commissure, and 
the adjoining portion of the optic thalamus (Wernicke). 

The treatment of the ocular paralyses is very problemati- 
cal, and rarely produces unquestionable results. Usually a 
trial is made with iodide of potassium, a course which may 
be justified if there is a history of syphilis ; but this drug is 
frequently of no avail whatever. Electricity is used either 
by applying one electrode over the closed lid of the diseased 
eye and the other over the base of the neck, so as to pass the 
current through the whole course of the eye muscles, or by 
allowing the current to pass transversely through the head 
from one mastoid process to the other. Medium-sized elec- 
trodes should be used and a weak current be applied about 
four times a week, each session occupying from one to two 
minutes. Now and again after prolonged galvanization we are 
really fortunate enough to perceive an improvement in the 
paralysis, or even to see it disappear. That much of this is to 
be attributed to the treatment seems doubtful, if we remember 
that it is utterly impossible to stimulate the ocular muscles 
with the current ; for the same reason an electrical examina- 
tion in ocular palsies is impossible (cf. Erb, Electrotherapie, 
page 428). 

Passing over the different spasms of the eye muscles which 
occur in some brain diseases, we shall pay attention here only 
to one form with which the neurologist ought to make himself 
familiar, viz., nystagmus. This consists in a to-and-fro motion 
of the eyeballs in a certain plane, usually horizontal {nystagmus 
oscillatorius), which continues on voluntary movements of the 
eyes, but which is itself not under the control of the will. 
These movements are usually present in both eyes, and vary 
quite markedly in frequency and extent, according as the pa- 
tient is made to fix a point or to change the direction in which 
he is looking. The condition is supposed to be due to weak- 
ness of sight of both eyes, dating from early childhood — that 
is, to impairment in the functions of the retina at a time when 
these have an important regulating influence in the establish- 
4 



5o 



DISEASES OF THE CRANIAL NERVES. 



ment of the normal fixation of the eyes (von Graefe). How- 
ever, there are undoubtedly cases which do not belong to this 
class, for it is a well-known fact that nystagmus may be a pro- 
fessional disease, as it is often observed in miners who have 
to use their eyes in the dark (Schroeter, Mooren, Nieden, 
Foerster, and others ; cf. also Hirt, Krankheiten der Arbeiter, 
Part II ; Die aeusseren Krankheiten der Arbeiter, page 189, 
Leipzig, 1878); and, secondly, it appears in the course of 
certain nervous diseases — perhaps in connection with repeat- 
edly occurring cerebral anasmia (Knoll, Ueber die nach Ver- 
schluss der Hirnarterien auftretenden Augenbewegungen — 
Sitzungsber. d. Akademie d. Wissenschaften in Wien, Abthei- 
lung III, 1886). In both these classes of cases sight is often 
not diminished at all, and some other than the one given above 
must be the underlying cause ; and, as a matter of fact, this 
nystagmus of the miners is simply due to overstrain of the eyes 
in an insufficient light, while the nystagmus occurring in the 
course of nervous diseases, more especially of multiple scle- 
rosis, but also of tabes and epilepsy, is to be regarded as a 
symptom and attributed to the same influences as the main dis- 
ease. That nystagmus, finally, may also be a symptom of hys- 
teria, and may persist during the whole course of the disease, 
is shown by a case lately published by myself (cf. Deutsche 
med. Wochenschr., No. 30, 1887, lit.). 

LITERATURE. 

Kahler and Pick. Zur Localisation central bedingter, partieller Oculomotorius- 

lahmungen. Arch. f. Psych, u. Nervenkr., x, p. 334, 1880. 
Lichtheim. Ueber nuclease Augenmuskellahmungen. Schweizer Corresp.-Bl., 

xii, 1, 2, 1882. 
Leeser. Die Pupillarbewegung in physiologischer und pathologischer Bezieh- 

ung. Wiesbaden, Bergmann, 1881. (With a complete list of references.) 
Blanc. Le nerf moteur oculaire commun et ses paralysies. Paris, Delahaye & 

Lecrosnier, 1886. 
Heddaeus. Die Pupillarreaction auf Licht, ihre Priifung, Messung und klinische 

Bedeutung. Wiesbaden, Bergmann, 1886. 
Parinaud-Juler. Paralysis of the Movement of Convergence of the Eyes. Brain, 

October, 1886. 
Mauthner. Die nicht nuclearen Lahmungen der Augenmuskeln. Wiesbaden, 

Bergmann, 1886. 
Mauthner. Die Nuclearlahmung der Augenmuskeln. Wiesbaden, Bergmann, 

1886. 
Schmidt-Rimpler. Beitrag zur Diagnose der Nuclearlahmung. Centralbl. f. 

prakt. Augenheilkunde, p. 276, 1886. 



DISEASES OF THE MOTOR NERVES OF THE EYE. 



51 



Mobius. Ueber die Localisation der Ophthalmoplegia exterior. Centralbl. f. 
Nervenheilk., ix, 17, 1886. 

Richter. Ein Fall von typisch recidivirender Oculomotoriuslahmung mit Sec- 
tionsbefund. Arch. f. Psych, und Nervenkrankh., xviii. 1, p. 259, 1887. 

Westphal. Ueber einen Fall von chronischer progressiver Lahmung der Augen- 
muskeln (Ophthalmoplegia externa) nebst Beschreibung von Ganglienzellen- 
gruppen im Bereiche des Oculomotoriuskernes. Arch. f. Psych, und Ner- 
venkrankh., xviii, 3, p. 846, 1887. 

Blanc. L'Ophthalmoplegie nucleaire. Arch, gener. de med., January, 1887, 

P- 57- 

Beevor. Ophthalmoplegia externa. Brit. Med. Journ., March 19, 1887. 

Lee, Henry. On the Functions of the Fourth Pair of Nerves. Lancet, Febru- 
ary 1, 1887, p. 9. 

Wattewille. Lahmung der Convergenzbewegungen der Augen im Beginn der 
Tabes. Neurol. Centralbl., No. 10, 1887. 

Kojewnikoff. Ophthalmoplegic nucleaire. Progr. med., No. 36, September 
1887. 

Suckling. Brain, xxxviii, p. 241, 1887. (Attacks of migraine, every time fol- 
lowed by paralysis of the third.) 

Senator. Ueber periodische Oculomotoriuslahmung. Zeitschr. f. klin. Med., 
xiii, 3, 4. P- 252, 1887. 

Salgo. Die unregelmassigen Reactionen der Pupillen. Wien. med. Wochen- 
schr., 45, 1887. 

Lemoine. De la blepharoptose cerebrale. Revue de med., vii, No. 7, 1887. 

Landolt-Magnus. Uebersichtliche Zusammenstellung d. Augenbewegungen im 
physiolog. und pathol. Zustande. Breslau, Kern, 1887. 

Sigaud. Progr. med., 36, 1887. (Assumes the cortical center of the third 
nerve to be situated in the angular gyrus. Autopsy.) 

Bull. Passive Motion in the Treatment of Paralysis of the Ocular Muscles. 
New York Med. Record, xxxii, August, 1887. 

Wadsworth. Ibid., August, 1887. (Recurring oculo-motor paralysis.) 

Remak, E. Doppelseitige Trochlearisparese. Neurol. Centralbl., 1888. 

Bernhardt. Beitrag zu der Lehre von den basalen und nuclearen Augenmuskel- 
lahmungen. Arch. f. Psych., xix, 2, p. 505, 1888. 

Mobius. Ueber angeborene doppelseitige Abducens-Facialislahmung. Miin- 
chener med. Wochenschr , 6, 1888. 



CHAPTER IV. 

THE DISEASES OF THE TRIGEMINAL NERVE. 

The trigeminus, the stoutest of all the cranial nerves, leaves the 
brain by two separate roots — an anterior small, exclusively motor, 
and a posterior larger, the sensory portion. Its point of exit is 
situated at the base of the pons, where the transverse fibres of the 
latter are prolonged into the middle peduncle of the cerebellum. 
Both roots lie in close apposition, and pass into a recess — the cavum 
Meckelii — formed by the dura mater, and situated over the inner 
end of the superior surface of the petrous portion of the temporal 
bone. Here the posterior root forms a somewhat crescentic swell- 
ing — the Gasserian ganglion — from which pass forward the three 
somewhat flattened divisions, the ophthalmic and the superior and 
inferior maxillary nerves, the last being joined by the smaller motor 
root. These three branches leave the interior of the skull by the 
sphenoidal fissure, foramen rotundum, and foramen ovale, respect- 
ively. 

The trigeminal nerve possesses two nuclei — a motor and a sen- 
sory one. The first — the smaller — is situated in the outer part of 
the tegmentum, and its ganglionic cells are characterized by their 
relatively large size (60 to 70 fx in the greatest diameter). The 
larger — sensory — nucleus lies external to the motor; in its collection 
of gray matter there are found very small ganglionic cells (20 to 30 /*, 
in diameter). 

With regard to the origin of the two roots there exist very 
different views, and but little is definitely known about the sub- 
ject. It can not be doubted that the motor root springs from what 
has been decided upon as the motor nucleus, nor that there exist a 
number of small bundles of fibres which arise high up in the region 
of the anterior quadrigeminal body, and descend outside the aque- 
duct to the level of the exit of the fifth nerve, where they help to 
form the motor root. This is the so-called descending anterior, or, 
as Henle terms it, superior root, the section of which, a crescentic, 
externally convex, internally concave figure, at once strikes the eye 
in frontal sections of the pons (cf. Fig. 9, Vd). That the sensory 



THE DISEASES OF THE TRIGEMINAL NERVE. 



53 



root arises from the above-mentioned sensory nucleus is probable, but 
not certain. On the other hand, it must be remembered that as low 
down as the neighborhood of the second cervical nerve there can be 
demonstrated in the caput cornu posterioris a layer of longitudinal 
medullated fibres, the highly characteristic transverse section of 
which, crescentic in shape, may be followed upward, as it gradually 
increases in size, as far as the level of the exit of the trigeminus. 
Suitable longitudinal sections plainly show that this longitudinal 
bundle forms a large part of the sensory root of the nerve. This is 
the so-called large ascending root of the fifth, the position of which 




V.s. 

Fig. ii. — Nuclei of the Trigeminal Nerve. (After Schwalbe.) n. V.s., nucleus of 
the sensory, n. V.m., nucleus of the motor root, d, fibres passing to the raphe. V.s., 
sensory root. 

in transverse section is represented in Fig. 12. The cortical area of 
the trigeminus is not definitely known as yet ; still, from experiments 
on animals, as also from the few clinical observations which we pos- 
sess, there is reason to conclude that at least so far as the motor 
portion of the nerve is concerned, it is located in the region of the 
anterior portion of the fissure of Sylvius; as regards the sensory por- 
tion we know nothing. 



We shall divide the affections of the trigeminus into cen- 
tral and peripheral. In the first class we recognize cortical 
and bulbar diseases ; in the second class we have to deal with 
either intra- or extra-cranial lesions. The trigeminus being a 
mixed nerve, containing in by far its larger portion only sen- 



54 



DISEASES OF THE CRANIAL NERVES. 




sory, but in its third branch important motor fibers, we are 
obliged, as there may exist in any case conditions of irritation 
n x ' n.am. or °f paralysis, to distinguish 

clinically between hyperses- 
thesia (neuralgia, neuritis) and 
anassthesia of the sensory part 
of the nerve, and between hy- 
perkinesis (spasm) and akine- 
sis (paralysis, paresis) of the 
motor portion. 

I. The Central Affections 
of the Trigeminus. 

In dealing with the corti- 
cal affections of the trigeminus 
we discriminate between irri- 
tative and destructive lesions 
of the cortical centre. In the 
former case we get spasm, in 
the latter paralysis of the mus- 
cles of mastication. 

Spasm of the muscles of 

mastication (trismus, mastica- 

fasdcuius). p, pyramidal tract, o, olive, tory facial spasm — Romberg) 

/.AT pyramidal nucleus, f.l.a anterior Ion- occurs frequently as a part 

gitudinal fissure. «.#;«, nucleus ambiguus. L J , r 

of general convulsions (Sena- 
tor, Petrina, Seligmiiller), and much more rarely indepen- 
dently, unaccompanied by other spasms (Lepine, Pfungen, 
v. Langer). There are two forms— a tonic, in which the 
teeth are pressed firmly together and the muscles of mas- 
tication, usually of both sides, are hard as wood to the 
touch ; and a clonic, in which the lower jaw is moved to and 
fro horizontally or vertically, and spasmodic masticatory move- 
ments are induced. In a case in my practice, in an old gen- 
tleman who had suffered from repeated slight apoplectic at- 
tacks, the patient for several hours every day goes through 
well-marked chewing movements without eating anything, 
which at times are so vigorous that he often while smoking 
bites through his cigar unintentionally. The origin of the 
disease is often of a reflex nature. Toothache, periostitis of 
the inferior maxilla, face-ache, may give rise to it. Sometimes, 
it may be, a cortical affection lies at the bottom of it, but for 



/■*■* * n'ar. 

Fig-. 12. — Cross-section through the Me- 
dulla Oblongata. (After Schwalbe.) 
a. V, ascending root of the fifth. n.XII, 
nucleus of the hypoglossus. n.X and n.X', 
nucleus of the vagus. XII, hypoglossal 
nerve, fs, solitary funiculus (respiratory 



THE DISEASES OF THE TRIGEMINAL NERVE. 



55 



this there is at present no evidence furnished by post-mortem 
examinations. 

Paralysis of the muscles of mastication is, on the whole, less 
frequently observed than spasm. Barlow, Oulmont, and Kirch- 
hoff report cases of it, recording in some only cortical lesions, 
but in others changes in deeper-lying portions of the brain as 
well. All the cases had this one anatomical feature in common, 
viz., that the cortical lesions always occurred bilaterally, thus in 
every case involving both centres. The first instance in which 
a unilateral lesion of the cortex was found was published by 
myself (cf. lit.). It confirms the supposition that the cortical 
motor area of the trigeminus includes the lower third of the 
anterior central convolution and the adjoining portion of the 
second and third frontal convolutions, and demonstrates that 
a unilateral lesion of the cortex (in this case it was left-sided) is 
sufficient to paralyze the muscles of mastication on both sides. 
The lesion was due to the presence of a psammoma the size of 
a filbert, which was situated upon the dura and cortex at the 
spot indicated, causing a depression and softening of the latter. 
The paresis of the muscles of mastication had reached a high 
degree, and was the more interesting from the fact that it was 
accompanied by periodical attacks of pain in the face and 
spasm in the area of distribution of the left facial nerve. Pa- 
resis and paralysis of the muscles of mastication are occasion- 
ally observed among the symptoms due to progressive bulbar 
paralysis and to pseudo-bulbar paralysis. The idea that these 
may develop as the result of a peripheral affection in an isolated 
disease of the motor portion of the third part of the trigeminus 
can not a priori be considered as impossible, but there have 
been up to the present no such cases observed. The differen- 
tial diagnosis between a central and peripheral affection could 
be made only by means of an electrical examination. The 
lesion is central if there are neither quantitative nor qualitative 
changes in the reaction to the faradic and the galvanic cur- 
rents. If such changes, however, exist — for instance, if there 
be the " reaction of degeneration " — the lesion is peripheral. 

Only the latter form of the disease is amenable to treatment 
(by electricity), and then with but slight chance of success. 
Against the central variety we are absolutely powerless. With 
regard to the affection of the nuclei and roots of the fifth nerve 
in the pons, the anatomical relations of which are, as we have 
seen, not as yet sufficiently well understood, we know little 



56 DISEASES OF THE CRANIAL NERVES. 

or nothing. Whether they ever occur independently, or, as 
is more likely, only as concomitants of diseases of other bul- 
bar nerve centres, has not been determined. However, the 
supposition seems justified that the centres in question, in the 
course of certain general diseases of the nervous system — for in- 
stance, in multiple sclerosis and particularly in tabes — are af- 
fected relatively early. Thus Erben reports (Wiener med. 
Blatter, Nos. 43, 44, 1886) that he has observed very trouble- 
some paresthesias of the sense of taste in tabetics occurring in 
paroxysms, beginning in the pharynx. These were especially 
pronounced at the anterior edge of the tongue, and were ac- 
companied by anaesthesia in the second branch of the fifth. 
This condition is presumably to be considered a disease of the 
nerve of taste, being analogous to the so-called gastric crises 
which are attributed to an affection of the vagus centre. A cen- 
tral anaesthesia of the trigeminus may also occur. In its symp. 
toms it would not differ from the peripheral except that it may 
be bilateral. The central nature of the trouble one would infer 
from the simultaneous participation of other nerves, both sensory 
and motor (Romberg). The interference with conduction may 
take place at the base of the brain. 

LITERATURE. 

Romberg. Lehrbuch der Nervenkrankheiten des Menschen. 3. veranderte 

Auflage. Berlin, 1853, p. 367 et seq. 
Senator. Berl. klin. Wochenschr., 4, 1879. 
Petrina. Prager Vierteljahrschrift. Bd. 133. 
Seligmuller, Archiv fur Psychiatric Bd. vi, p. 825. 
Gerhardt. Festschrift der Wiirzburger Universitat. Leipzig, 1882. 
Barlow. Brit. Med. Journ., July 28, 1877. 
Oulmont. Revue mensuelle, 1877. 
Kirchhoff. Arch. f. Psychiatric Bd. xi, p. 1 33. 
Hirt. Zur Localisation des corticalen Kaumuskelcentrums beim Menschen. 

Berl. klin. Wochenschr., No. 27, 1887. 

II. Peripheral Affections of the Trigeminus. 
In its peripheral part the nerve may become diseased inside 
as well as outside of the cranium. If the lesion is one of the 
stem, and extends to all three branches, it may be difficult, in- 
deed impossible, to determine its exact site, because we do not 
as yet possess any means which enable us to definitely decide 
whether the nerve is diseased centrally from the Gasserian 
ganglion, whether the ganglion itself, or, finally, whether the 



THE DISEASES OF THE TRIGIMINAL NERVE. 57 

three individual branches are all affected at their exit from the 
skull. 

An affection of the nerve stem to the central side of the 
Gasserian ganglion can only be assumed with any degree of 
certainty if the nerve is diseased in its whole sensory distri- 
bution and if extensive trophic disturbances are also present. 
The affections of the Gasserian ganglion itself (inflammation, 
neoplasm, softening) have as yet but little practical importance. 
If the disease does not take in the stem, but only the terminal 
portions of the individual branches, it is easy to determine the 
seat, and while we have in the intracranial diseases to consider 
those of the finer branches of the nerve in the dura, in the ex- 
tracranial we have the branches distributed to the face and 
those to the nasal cavity. 

A. Intracranial Diseases. 

HeadacJie — Cephalalgia — Migraine — Hemicrania. 

Since it is very likely that there are only exceptional cases 
of idiopathic headache in which the fifth or its terminal 
branches in the dura (cf. page 3) are not implicated, it seems 
advisable to speak of headache here. At the same time we 
must expressly state that we are forced thus to take up differ- 
ent diseases together, which are astiologically as well as patho- 
logically to be strictly separated from one another. 

The main point to decide in a given case will always be 
whether the headache is to be regarded as merely a symptom 
of another disease or as an affection by itself. Nobody ever 
would assume a headache which occurs at the onset of a severe 
illness — for instance, an acute infectious disease, or in associa- 
tion with organic brain disease (e. g., tumor), or during grave 
disorders of nutrition, anaemia, and chlorosis — to be an affec- 
tion by itself and treat it as such. These headaches will 
always be considered as a mere symptom of the underlying 
disease ; but when we find an otherwise healthy person suffer- 
ing from protracted or paroxysmal headache, while on repeated 
careful examination we are unable to discover any other dis- 
ease, then we are forced to assume an independent affection 
and we have to endeavor to determine the following points : 
(a) The seat of the headache ; (b) its peculiarities and its course ; 
(c) its aetiology ; {d) its appropriate treatment. 

Pathology. — The anatomical situation of the headache can 



58 



DISEASES OF THE CRANIAL NERVES. 



hardly ever be determined ; but we are justified, since we do 
not know what part the brain substance takes in it, in believ- 
ing that the sensory terminal branches of the trigeminus in the 
dura (the dura receives at least two branches from the tri- 
geminus) are always implicated, and are thus in some measure 
the seat of the headache. Under what conditions these nerve 
endings are thrown into a state of irritation — a state upon which 
the headache depends — is not well understood, and all we know 
about this question is more or less hypothetical. The most prob- 
able explanation is that the amount of blood in the brain or its 
membranes at the time being is an important factor in the pro- 
duction of the morbid condition, whether there be a permanent 
increase or decrease or frequent, perhaps very slight, changes in 
the amount. An increase constitutes what is called cerebral hy- 
perasmia, a decrease cerebral anaemia ; and we assume the former 
condition if full-blooded individuals, who are liable to rushes of 
blood to the head, complain of paroxysmal headache ; the latter, 
if it occur in pale, anaemic patients who are subject to fainting 
spells. However, we do not know anything positive, and we 
shall have occasion to deal more in detail with this in another 
place. Of the greatest interest, and perhaps of the most com- 
mon occurrence, are the fluctuations in the intracranial blood 
pressure, which possibly are the cause of the irritation of the ter- 
minal branches of the trigeminus in the dura and pia. If such 
fluctuations appear frequently, so as to give rise to an unequal 
distribution of the blood in the two halves of the brain, the 
irritability of the sensory endings may become abnormally in- 
creased, so that slight causes are sufficient for the production 
of the pathological condition. The clinical observations even 
go to show that without any demonstrable cause from time to 
time there may develop an increased irritability of these ter- 
minal branches of the fifth, associated with simultaneous fluctua- 
tions in the blood pressure. If the attack of headache thus pro- 
duced is accompanied by vaso-motor symptoms, either of a para- 
lytic or of an irritative nature, it is designated as migraine or 
hemicrania, the latter name being given to those not very com- 
mon cases in which the pain is strictly confined to one side of 
the head. Owing to the vaso-motor disturbances just men- 
tioned, some have been inclined to locate the seat of the disease 
in the sympathetic system, without being able, however, to 
show that the symptoms referable to the sympathetic are not 
perhaps only a secondary result of the pain, and therefore reflex 



THE DISEASES OF THE TRIGEMINAL NERVE. 



59 



in nature (Mobius) ; and until this is actually demonstrated not 
to be the case we are justified in looking- upon migraine as be- 
longing to the affections of the trigeminus. In some, as it 
seems, quite exceptional cases, the seat of the headache is to 
be referred to certain muscles, which present at their origin 
and insertion as well as in their course points of tenderness 
(O. Rosenbach, cf. lit.). Among these, besides the frontal oc- 
cipital and temporal muscles, are the sterno-cleido-mastoid and 
the upper part of the trapezius. This myalgia, which is occa- 
sionally produced by an unnatural position during sleep, and 
which is easily diagnosticated on careful examination, is said 
under certain circumstances to be the cause of headache. 

Symptoms and Course. — With regard to the peculiarities 
and the course of the headache connected with affections of the 
trigeminus, we know that in its character as well as in its situa- 
tion it presents no inconsiderable number of variations : thus, 
while one patient complains of a dull, boring ache, another de- 
scribes his pain as sharp and burning; while in the one it is 
worst in the forehead, another refers it chiefly to the occiput, 
vertex, or temples, etc. In some instances the patients designate 
sharply circumscribed places of the hairy scalp as the seat of their 
pain. The headache also varies much in degree — from a dull 
sensation of pressure to a pain which allows of no sleep. In some 
cases the suffering is increased by a touch or a tap on the head, 
while in others it is soothed by a firm bandage around the tem- 
ples. But seldom do we find a headache lasting for days, weeks, 
or even months without interruption ; usually there are times 
when it is less severe or when it ceases completely. There is 
no regularity or uniformity in the occurrence or duration of 
the attacks. Two cases are scarcely ever alike, and almost al- 
ways each presents certain peculiarities of its own : thus in the 
one slight febrile movements, absent in another, may occur ; 
one patient enjoys a splendid appetite during the most violent 
pain, while another is unable to eat a thing, etc. The so-called 
attack of migraine has, at least in some cases, certain character- 
istics of which we shall now speak. It is usually for several 
hours preceded by prodromal symptoms, general lassitude, 
chilly feelings, tendency to yawning, buzzing in the ears, and 
the like. If the regular attack is going to begin in the morn- 
ing the patient wakes up repeatedly during the night, and is 
thus able to predict the attack with certainty. The headache 
is sometimes, as we have remarked above, confined to one side, 



60 DISEASES OF THE CRANIAL NERVES. 

and, according to statistics, the left seems to be the one pre- 
ferred ; but the seat often changes during the attack, so that 
the patient complains now of the left, now of the right side of 
the head. Sometimes a distinct pallor is noticeable on one side 
during the attack, associated with dilatation of the pupil and 
increase in the salivary secretion, while in other instances one 
half of the face is flushed and hot, the arteries pulsating strong- 
ly, and the pupil contracted. In the first case we designate 
the hemicrania as spastic (sympathico-tonica, connected with 
stimulation of the sympathetic); in the latter as paralytic (con- 
nected with paralysis of the sympathetic). The former has 
been described by Du Bois-Reymond, the latter by Mollen- 
dorf, in both cases after observations made upon themselves. 
But these conditions are not constant either, and if one has 
seen many attacks of migraine he knows full well that the pa- 
tients often change color — they are now pale, now flushed, 
now complain of a feeling of heat in the head, now of cold. 

If the pain is very violent the patient shows general consti- 
tutional symptoms. In a bad attack he lies for hours com- 
pletely apathetic, meeting every question and every source of 
disturbance with unmistakable signs of disgust. He refuses 
nourishment entirely, owing to a feeling of utter discomfort 
and an almost uncontrollable desire to vomit. Only after copi- 
ous vomiting of bile-like mucoid masses does his condition 
gradually improve, the amelioration beginning with a violent 
desire for food and a polyuria following the attack, which is 
finally ended by a refreshing sleep. When vomiting does not 
occur the patient suffers for a longer period of time. Some- 
times the eyes participate, and photophobia, flitting scotomata, 
even hemianopia, have been observed during the attack. These 
are instances of what Fere calls migraine ophtlialmique, a form 
which he carefully discusses in his admirable monograph on 
the subject. It is not uncommon for the attacks not to reach 
their full development, but only for certain symptoms — flitting 
scotomata, vomiting, vaso-motor disturbances, or the like — to 
appear. Such isolated symptoms may be called " hemicranic 
equivalents " (Mobius). 

The duration of the attack varies from a few hours to a 
whole day ; it rarely lasts longer, and if it does, this fact should 
always make us doubtful as to the diagnosis. In the intervals 
the patients as a rule feel well ; still, if the attacks are very se- 
vere and frequent, occurring, for instance, as often as once or 



. THE DISEASES OF THE TRIGEMINAL NERVE. 6 1 

twice a week, the after effects may be so lasting that the suffer- 
ers never can enjoy perfect health. Fortunately, such a rapid 
succession of the seizures is uncommon. Once a month or six 
or eight times a year is the rule, not counting slight, abortive 
attacks. 

The course of migraine is always extremely tedious, some- 
times lasting through a whole lifetime. In women the climac- 
teric period occasionally, but by no means always, exerts a 
beneficial influence. At the time of menstruation the attacks 
seem to be especially apt to occur ; but, even if no definite at- 
tack makes its appearance, women who are subject to migraine 
complain of more or less severe headache at such periods. Not 
infrequently the disease has an unfavorable influence on the 
disposition and appearance of the patients ; they become pee- 
vish and ill-tempered, and even in the intervals between the 
attacks are by no means amiable or sociable. They are wont 
to restrict themselves considerably in their social intercourse 
— for one reason, because they rarely are able to make engage- 
ments for definite times, on account of the possibility of the 
occurrence of one of their attacks. The trophic disturbances 
which are sometimes superadded, as, for instance, the prema- 
ture gray hairs, make such patients look older than they really 
are ; on the other hand, there are individuals who, notwith- 
standing the severity of the attacks, retain for a long time their 
youthful freshness and vivacity. This may especially be hoped 
for if in the intervals the patients enjoy sound and healthful 
sleep. Unfortunately, in the majority of cases they are de- 
prived of this, and are forced to resort to artificial means to 
procure it, of which the bromides are the most popular. It is 
not always easy to understand the cause of the sleeplessness 
{agrypnid) in migraine, and for that matter in all nervous dis- 
eases ; it is especially difficult to do so when this is the only 
symptom and absolutely nothing else can be detected, when 
individuals otherwise healthy are wholly or almost wholly de- 
prived of sleep for weeks ; and yet it is just the discovery of 
this primary cause that is of the greatest importance, as it will 
guide our action in the treatment; and only when this is found 
can we reasonably hope for improvement from our efforts. 
Sometimes we have to deal with a gastric catarrh which until 
this time has been overlooked, a hyperasmia of the liver, and 
the like, and after the successful treatment of these by Carlsbad 
water, etc., sleep, which in spite of all bromides and morphine 



6 2 DISEASES OF THE CRANIAL NERVES. 

had in vain been sought, returns of its own accord. Some- 
times a high grade of angemia may lie at the bottom, easily 
recognizable by the pallor of the skin, the small pulse, and 
the cold extremities. In such cases cod-liver oil, iron, and 
quinine are more serviceable than the usual hypnotics, which 
are rarely well borne. In all nervous patients suffering from 
insomnia it is advisable to examine the thoracic and abdominal 
as well as the sexual organs, and only to treat the sleeplessness 
symptomatically when repeated examinations have given nega- 
tive results. This symptomatic treatment consists above all in 
the careful use of massage, which should be supervised by the 
physician, a practice from which we have obtained very grati- 
fying results. Next comes the systematic galvanization of the 
brain, for the technical details of which the reader is referred 
to Erb's book on electro-therapeutics (page 333, Leipsic, 1882). 
As a last resort we have the administration of quieting, calm- 
ing, and sleep-producing drugs, among which, notwithstanding 
all the new hypnotics, morphine still holds the first place. Be- 
sides this, chloral, paraldehyde, urethan, hypnone, coniine, lupu- 
line, and amylene hydrate (tertiary amyl alcohol), which has 
recently been recommended by von Mering, may be tried. 
The latter is best given in doses of three and a half to four 
grammes (-r^l-lx) in one dose once in twenty-four hours, and 
seems often to have a favorable action. On account of the bad 
taste of this drug the addition of correctives — for instance, the 
oil of peppermint, which somewhat masks the taste — is to be 
recommended. (Amylene hydrate, 7.0 (tticv) ; aq. menth. pip., 
40.0 (3x);.ol. menth. pip., 1.0 (ttixv) ; syrup, simpl., 30.0 (5j)- 
Sig. : Half to be taken at night.) The sleep after it is deep and 
quiet, and unpleasant after-effects are rare. Nevertheless, it is 
well to be careful in its administration, as symptoms of intoxi- 
cation may appear, as Dietz has reported (Deutsch. Medicinal- 
Zeitung, 1888, 18). Migraine is frequently complicated by 
stomach troubles, and more especially by cardialgia (gastral- 
gia), and the peculiar form of nervous dyspepsia which Ross- 
bach has called " nervous gastroxynsis " (yaar^p d£v<i). Of car- 
dialgia we shall speak in discussing the neuroses of the vagus, 
and it suffices here to mention that it is often associated with 
slowing of the pulse, meteorism, flatulence, and vomiting. The 
gastroxynsis, which depends upon an abnormal increase in the 
production of free hydrochloric acid, begins with an extremely 
disagreeable feeling of acidity in the stomach, with severe, at 



THE DISEASES OF THE TRIGEMINAL NERVE. 63 

times intolerable, headache, and ends with the vomiting of 
large strongly acid masses. That the headache in these cases 
does depend on the acidity of the stomach is evident from the 
following reasons (Rossbach) : (1) It ceases when the acid mass- 
es are thrown off or if they are diluted by copious draughts of 
warm water ; (2) in persons suffering from gastroxynsis it often 
appears after indulgence in acid food — e. g., salads. It may in 
general be put down as a fact that by far the greater propor- 
tion of sufferers from habitual headache or migraine have at 
the same time some trouble with the stomach ; the frequent 
belching, the loss of appetite, the foul breath, speak in favor of 
this, and no one of these three symptoms is scarcely ever ab- 
sent in patients of this class. 

iEtiology. — ^Etiologically headache and typical migraine 
have much in common; heredity, above all, the influence of 
which is so striking in migraine, plays an important part. It 
need not be of necessity the parents who have been affected ; 
often the grandparents or their sisters or brothers or the uncles 
and aunts may have suffered from it ; and we should therefore, 
in getting the family history of the patient, carefully inquire 
into the health of such relatives. Only in patients with heredi- 
tary tendency have we observed migraine in childhood — in girls 
of from six to seven years of age — as in other cases it develops 
as a rule during puberty. Young, rapidly growing individu- 
als who have to do hard rhental work (preparation for exami- 
nations, etc.) are frequently sufferers from severe migraine 
{Jiemicrania adolescentiitni). The influence of the stomach on 
the development of the disease has already been spoken of. 
As a matter of fact, habitual headache or typical migraine is 
often developed after repeated excessive indulgence in indi- 
gestible food ; more frequently, it is true, the stomach and 
head symptoms are developed together. Quite recently Legal 
has called attention to the fact that, especially in cases where 
the headache is referred to the temples or to the occipital re- 
gion, the underlying cause is frequently to be found in diseases 
of the middle ear and the pharynx. He advises in such cases, 
after a careful examination, the use of Politzer's inflations. 

The serological importance which has to be attributed to 
errors in accommodation or refraction, more especially to 
hypermetropic astigmatism, has been pointed out by A. Bick- 
erton (cf. lit.). There is no doubt but that in very exceptional 
cases migraine has to be looked upon as a reflex neurosis, 



64 DISEASES OF THE CRANIAL NERVES. 

which is caused by chronic uterine or intestinal disturbances 
(worms, taenia), and we should take this possibility into con- 
sideration in our search for the cause. Exceptionally, migraine- 
like attacks have been observed in the course of gout, and it 
looks as if they were also in some way connected with the 
excretion of uric acid, since it has been found that before the 
attack no uric acid can be detected in the urine, while after it 
the amount is very markedly increased and, later on, for a time 
considerably diminished. The polyuria which occurs frequent- 
ly after the attack, and lasts for several hours, where an acid 
urine, light yellow, almost as clear as water, of a very low 
specific gravity — 1.005 to 1.007 — is voided, has before been men- 
tioned, and to the fact that migraine-like attacks may also 
occur in the initial stage of tabes, and may be of importance 
for the diagnosis and prognosis, we shall have to refer later. 

Prognosis. — It is difficult, indeed at times impossible, to 
give a reliable prognosis in the cases now under consideration. 
So far as life is concerned it is always favorable if the case is 
one of a purely functional disturbance — that is, where the head- 
ache or migraine exists by itself as an independent affection, 
and where it is not to be regarded as a symptom of another 
disease. Life in such cases, as we said, is never in danger ; 
the patient recovers from his severest attacks comparatively 
readily, and even after frequent repetitions of them it is excep- 
tional that the digestive disturbances and the loss of strength 
which these entail give rise to a serious condition. But is the 
prognosis for recovery as good as for life ? To this question 
we must answer without reservation, No. One can not deny 
that the outlook for a complete recovery is on the whole very 
bad, and that the chances, cceteris paribus, are so much the worse 
the longer the disease has lasted, and the more difficult it is to 
find any tangible cause. The worst cases are those where the 
trouble is inherited ; in these recovery is very exceptional. 
At any rate the prognosis in all cases should be guarded, and 
little should be promised. There is hardly any other disease 
which is so liable to injure the physician's authority and the 
patient's faith in him and his medical skill as migraine and 
habitual headache. On the other hand, spontaneous recover- 
ies are not unheard of, a fact which we ought to remember if 
all our drugs leave us in the lurch. 

Treatment. — The treatment of habitual headache, and espe- 
cially of migraine, is generally very tedious, and puts to a severe 



THE DISEASES OF THE TRIGEMINAL NERVE. 65 

test the perseverance, not only of the patient, but also of the 
physician. It is, therefore, an absolute necessity before under- 
taking to treat a patient of this kind to lay down, after a most 
careful and minute examination, a definite plan of treatment, 
which must be rigorously adhered to. It is not sufficient to 
use to-day this, to-morrow that drug, of which we have possi- 
bly read in the last journal as being effectual against migraine, 
and with which we may accidentally obtain a transient good 
result, but the treatment must rather be systematic, and be the 
outcome of certain well-considered conclusions, which we shall 
now briefly discuss. In the first place, we have to decide 
whether there exists another disease which causes the migraine. 
If, as is frequently the case, stomach symptoms are present, a 
stay at Carlsbad or Kissingen may do much good. If the acid- 
ity of the gastric juice is increased, the regular ingestion of 
alkaline drinks or lukewarm water is indicated. In all cases 
much attention is to be paid to the diet, and patients should 
especially be warned against overloading their stomachs at 
night. The regulation of the bowels is effected by the use of 
large enemata of water, or of small ones of pure glycerin (5 to 
6 cc. (tti lxxx-c) at a time), or by vegetable aperients, such as 
rhubarb. Any degree of constipation may be attended with 
bad consequences. Diseases of the middle ear or the pharynx 
should be treated by a specialist. If the patient have a gouty 
diathesis, the use of lithium and the regulation of the diet 
should constitute the main treatment. The eyes should be 
examined for errors of accommodation and refraction which 
may exist, and these when found should be corrected by proper 
glasses. Cases which had resisted all other treatment have been 
cured in this manner (Bickerton, Brailey, Weir Mitchell, etc.). 

If no other co-existing diseases can be detected, our chief 
efforts must be directed to building up the general constitu- 
tion. From the cold-water treatment, general faradization 
(according to Beard and Rockwell), franklinization with the 
Holtz machine, systematic gymnastic exercise at home — from 
any one of these measures we may, under certain circum- 
stances, obtain the desired result. In some cases lasting ad- 
vantage has been seen from a change of climate, traveling, a 
stay in the mountains or at the sea-side. 

With regard to the combating or the shortening of the 
attack we may say that, although there are quite a number of 
drugs more or less warmly recommended, we should not ex- 

5 



66 DISEASES OF THE CRANIAL NERVES. 

pect too much from them. Two or three times they may be 
useful, but after repetition they lose their effect. If the above- 
mentioned vaso-motor changes point to the existence of a 
pathological contraction or dilatation of the blood-vessels we 
may, in the former case — in that of contraction — resort to the 
careful administration of nitrite of amyl, three to five drops of 
which are put on a handkerchief and given the patient to in- 
hale, or to the internal use of nitroglycerin (three times a day 
one drop of a one-per-cent alcoholic solution). Great care has 
to be exercised in the exhibition of the latter drug, and, if the 
pulse indicate it, we ought to begin with minimum doses. Such 
a precaution is more especially necessary if the pulse is full 
and the arterial wall tense, in which case a quarter or half a 
drop is sufficient as an initial dose (Trussewitsch). It is, more- 
over, not advisable to continue its administration any longer 
than one or two weeks, as it is liable to give rise to cerebral 
symptoms (buzzing in the head, vertigo). In the second 
case — that of vaso-dilatation — ergot is indicated, which may 
either be used in the form of hypodermic injections of ergotin 
(ergotinum dialysatum, i.o(grs. xv); aquae destill., 4.0 (3 j). Sig. : 
Half a syringeful), or by the mouth (extr. secal. corn. [Denzel], 
2.0 (tti xxx) ; aquas cinnamomi, 180.0 (^ vj). Sig. : A tablespoon- 
ful every two hours). Lately Kraepelin has recommended the 
hypodermic use of cystisin (0.003 to 0.004 (g r - V20 to gr. J / l6 ). — 
Neurol. Centralblatt, 1, 1888). If no such indications are fur- 
nished by the condition of the blood-vessels we have to try 
which medicine does the most good, and may begin with the 
citrate of caffeine (0.15 (about 2 grs.) three times a day), which 
we have in all cases found to be more effectual than the aethoxy- 
caffeine recommended by Filehne. If the latter is given in 
doses of 0.25 (about 4 grs.), as Filehne advises, it will induce 
violent vomiting, and the patients are worse than before. If, 
on the other hand, it is given in small doses, it is of no use — at 
least in no single case have we seen lasting benefit derived from 
it — whereas caffeine often does good service for months. The 
pasta guarana in 2.0 (grs. xxx) doses twice a day gives similar 
results, but often interferes with digestion. Salicylic acid is in 
many cases, especially at the onset, followed by surprising re- 
sults, but its continued use is disagreeable to the patient on 
account of the bad after-effects. I myself have never seen any 
remarkable results from antipyrine, which has recently been 
recommended, among others by Germain See (5.0 (grs. lxxv) 



THE DISEASES OF THE TRIGEMINAL NERVE. 



6 7 



in two hours). The action which antifebrine has in migraine 
has not as yet been carefully studied, but this drug certainly 
should be tried. Application to the painful spot of an alco- 
holic solution of menthol (three to twenty) is often both agree- 
able and refreshing to the patient, the migraine pencils also 
prepared with menthol having a similar effect. If painful 
points can be discovered on the scalp or on the muscles {vide 
supra), a slight pressure and kneading of the same, later a more 
energetic massage to the head, is advisable. 

Electricity may be used (i) in the form of the constant cur- 
rent passed longitudinally or transversely through the head or 
by applying it to the cervical sympathetic, and (2) in the form 
of the faradic current. In this case it is best for the physician 
to apply his own hand, previously moistened, to the forehead of 
the patient, this taking the place of one electrode. In the other 
hand he holds one of the electrodes, the other being placed on 
the back of the patient's head, the sternum, or some other in- 
different point. With this mode of application, which is called 
the "faradic hand," only very mild currents should be used 
(cf. Erb, Handbuch der Electrotherapie, page 327, Leipzig, 
1882). 

Numerous as are the means at our disposal for combating 
the disease, quite as numerous are the patients who, after hun- 
dreds of unsuccessful trials, give up all medicines and all physi- 
cians. They retreat at the beginning of the attack from the 
world and from their families, darken their rooms, lie down 
quietly, and take simple domestic remedies, among which Rus- 
sian tea with lemOn juice has obtained a prominent place. Ab- 
solute rest is what always does most good to all these patients. 
Finally, we should not forget to deprecate, especially here, 
the use of all hypnotics, more particularly morphine, as they 
never do any good, and are often capable of producing serious 
harm. 

LITERATURE. 

Briigelmann. Ueber Hemicrania spastica. Berliner klin. Wochenschr., 16, p. 

242, 1883. 
Keller. De la cephalee des adolescents. Arch, de neurol., 16, 17, 1883. 
Fere. Revue de med., 3, 1883. 

T. Clifford Allbutt. Neuroses of the Viscera. Lancet, i, u, 12, 14, 1884. 
Rossbach. Nervose Gastroxynsis als eine eigene, genau charakterisirbare Form 

der Dyspepsie. Deutsches Arch. f. klin. Med., xxxv, p. 383, 1884. 
Filehne. Das Aethoxycoffei'n als Substitut des Coffefns bei Migrane. Arch. f. 

Psych, und Nervenkrankh., xvii, 1, p. 273, 1886. 



68 DISEASES OF THE CRANIAL NERVES. 

Storch, 0. Remarques sur l'etiologie et la therapeutique de la migraine et de la 
cephalalgie nerveuse. Congr. intern, de Copenhague. III. Psych, et Neu- 
rol., p. 151, 1886. 

Rosenbach, O. Ueber die auf myopathischer Basis beruhende Form der Mi- 
grane und iiber myopathische Cardialgie. Deutsche med. Wochenschr., 12, 
13, 1886. 

Legal. Ueber eine oftere Ursache der Schlafe-Hinterhauptskopfschmerzen. 
Deutsches Arch. f. klin. Med., xl, 2, 1887; Bresl. arztl. Zeitschr., viii, 20, 
1887. 

Haig. Lancet, May 28, p. 1088, 1887. 

Eulenburg. Zur Aetiologie und Therapie der Migrane. Wien. med. Presse 
1887. 

Faust, W. Antifebrin gegen Kopfschmerz. Deutsche med. Wochenschr., No. 
26, 1887. 

Thomas. La Migraine. Paris, Delahaye, 1887. 

Bickerton. On Headache due to Errors of the Refractive Media of the Eye, 
Lancet, August 13, 1887, p. 303. 

Strumpell. Krankheiten des Nervensystems. 4. Aufl. Leipzig, 1887. 

Trussewitsch. Ueber Anwendung und Dosirung des Nitroglycerins als Arznei- 
mittel. Petersburger med. Wochenschr., No. 3, 1887. 

Mizller-Lyer. Lleber ophthalmische Migrane. Berliner klin. Wochenschr., No. 
42, 1887. 

Gilles de la Tourette et P. Blocq. Sur le traitement de la migraine ophthalmique 
accompagnee. Progr. med., No. 24, 1887. 

Glasgow. Boston Med. and Surg. Journ., cxvi, June 24, 1887. 

Grout. De la migraine dentaire. Gaz. des Hop., 106, 1887. 

Suckling. Brain, xxxviii, p. 241, 1887. 

B. Extracranial Lesions. 

The extracranial lesions are, on account of their great fre- 
quency, of an eminently practical significance and of scientific 
importance, inasmuch as valuable information about physiolog- 
ical questions — that is, the course of the trophic and the gusta- 
tory fibres — may be gained from them if the individual cases 
are carefully observed and accurately recorded. We shall 
have to treat of (1) the diseases of the facial branches of the 
nerve, and again separate in our consideration the paralytic 
from the irritative affections. 

/. Trigeminal Neuralgia — Fot her gill 's Face-ache — Tic Douloureux 
— Prosopalgia. 

Variable in its degree of intensity, beginning with a moder- 
ate, dull, boring, but always distressing and uncomfortable feel- 
ing of pain, and sometimes reaching a pitch of severity experi- 
enced in no other kind of neuralgia, tic douloureux forms one 



THE DISEASES OE THE TRIGEMINAL NERVE. 6g 

of the most common affections of the fifth nerve. It appears, 
as a rule, unilaterally, and by preference fastens upon the first 
and second branches. The sensory division of the third branch 
seems, at least by itself, rarely to be the seat of the pain, 
whereas it is not uncommon for all three divisions to be simul- 
taneously attacked. 

Almost every patient gives a different description of his 
pain. One declares that it feels as if a red-hot wire was being- 
driven into the bone, another as if the face was buried in a 
heap of stinging nettles, a third fancies that the nerves are be- 
ing pierced with a sharp instrument, etc. Almost every case 
presents its own peculiarities as regards the frequency and 
duration of the paroxysms, between which there are often inter- 
vals free from pain, but the course of the disease follows no 
hard and fast rules. The tender points of Valleix {points dou- 
loureux) can almost invariably be demonstrated. Almost al- 
ways there is one on the supra- and another on the infra-orbital 
foramen, a third over the exit of the subcutaneus malas, a 
fourth over the mental foramen, and a fifth in front of the ear, 
where the auriculo-temporal passes over the zygomatic arch. 
The so-called palpebral point on the upper eyelid, the parietal 
point on the parietal eminence, the labial point on the upper 
lip, and many others are not always present. Firm pressure 
on these points is always, even in the intervals between the 
paroxysms, disagreeable to the patient and even liable to pro- 
duce an attack. 

The neuralgia of the first division of the fifth nerve is mostly 
an affection of the supra-orbital nerve, with pain in the fore- 
head, the nose, the upper eyelid, and the eyeball (ciliary 
nerves). The other terminal branches are hardly ever affected. 
The neuralgia of the second division attacks the cheek, the 
lower eyelid, the nose, and the upper lip, often also the upper 
row of the teeth (n. alveol. sup.) and the palate (spheno-palatine 
branch). The branch most commonly affected, sometimes also 
by itself, is the infra-orbital. The neuralgia of the third division 
embraces the lower jaw, the chin, the cheek, sometimes also 
the auricle and the external meatus. The lower row of teeth, 
the tongue, and the mucous membrane of the mouth are often 
the seat of intense pain. As we have said, an isolated affec- 
tion of this third division is comparatively rare. The infe- 
rior alveolar branch, however, forms an exception to this, as 
it is not rarely attacked separately, and the consequent tooth- 



yo 



DISEASES OF THE CRANIAL NERVES. 



ache has often induced patients to have one tooth after another 
extracted — of course, however, without any improvement. 

That the vaso-mofcor and the trophic fibres of the nerves are 
also at times implicated is evident from certain symptoms, viz., 
intense flushing, hyperidrosis, strong pulsation of the temporal 
artery on the diseased side, together with increased secretion 
of tears and saliva, affections of the hair, which has a tendency 
to turn gray and fall out, especially over the most painful 
places. Such symptoms are not uncommon. Herpetic erup- 
tions, especially zoster ophthalmicus and frontalis of the af- 
fected side, have repeatedly been described. 

Pathology. — Of the pathology little can be said with cer- 
tainty. The thickening and swelling of the neurilemma, the 
degeneration of the Gasserian ganglion and of the nerve trunks, 
the small inorganic concretions which have occasionally been 
seen on the neurilemma — all these are changes which have 
sometimes been observed, but which quite as often were ab- 
sent. At all events no particular importance can be attributed 
to them. Whether cortical lesions and affections of the nuclei 
and the roots are capable of bringing on the disease we do not 
definitely know, yet such possibilities can not be excluded (cf. 
the case published by myself in the Berl. klin. Wochenschr., 
1887, 27). 

Course.— The course of the disease is on the whole extreme- 
ly tedious, and attacks which harass the patient to the end of 
his days are to be observed here as in migraine, the only differ- 
ence being that in the disease under consideration the suffer- 
ings of the patient are still more unbearable. The disease 
throws a shadow over his whole existence far more gloomy 
than in migraine, and so we can well understand why again 
and again he tries all sorts of remedies and frequently even 
the most heroic measures to relieve his pain at a time when a 
migraine patient would have given up all medicine and all 
doctors. 

Treatment. — Unfortunately, here also therapeutics is often 
powerless, as has already been indicated by the remark that the 
disease is often of life-long duration. Hope of recovery is only 
justifiable in cases where we have an underlying disease, as, for 
instance, malaria, in which case the neuralgia is to be regarded 
as a symptom, or where local causes exist — for instance, bone 
diseases, the presence of foreign bodies, or neoplasms which 
can be removed, etc. Such cases will repay the efforts of the 



THE DISEASES OF THE TRIGEMINAL NERVE. 



n 



physician, and a cure can be effected by proper internal medi- 
cation or by surgical interference. In cases, however, where a 
primary cause, which would furnish vis with data for our treat- 
ment, can not be discovered — where we, therefore, are forced 
to experiment with the nervines and the so-called specifics — let 
us beware of raising our expectations too high, for too often 
all our efforts will be in vain. Arsenic, zinc, quinine, the bro- 
mide and iodide of potassium, asafcetida, castoreum, valerian, 
and many other medicines now completely obsolete have been 
tried, and still to-day sometimes are tried at random. The one 
uses this, the other that drug ; under favorable circumstances 
each one does good once, but rarely is the improvement last- 
ing. The most confidence may be placed in iron, if chlorosis 
be present (best administered in the form of Blaud's pills), qui- 
nine, arsenic, and iodide of potassium ; if these leave us in the 
lurch we can resort to salicylate of sodium, 4.0-6.0 (3 j— 3 jss.) a 
day, in capsules, or to salol or gelsemium, giving the latter in 
the form of the tincture, and pushing it perhaps until slight 
symptoms of intoxication appear (twenty drops every two 
hours). I have used corrosive sublimate, 0.05 (five-sixths of a 
grain a day) in pill form, several times successfully. Of butyl- 
chloral I am unable to say anything favorable (butyl chloral 
hydr., 7.5 ( 3 jss.— 3 ij) ; glycerin., 20.0 (§ ss.) ; aquae, 130.0 (§iv). 
Sig. : A tablespoonful every ten minutes). In all my cases it 
proved very unsuccessful ; the same holds good for bichlorate 
of methylene, which is applied externally in the form of a 
spray. Other anaesthetics, chloroform above all, do at least as 
much good, and the narcotics are decidedly better, as Trousseau 
has already upheld, who declared large, or we should rather 
say huge, doses of opium or morphine to be the only effectual 
treatment. Whatever we may think about morphine, in cases of 
tic douloureux, especially in severe instances, we can not dis- 
pense with it. The combination of morphine with atropine, or 
the alternate use of the two separately, has been recommended 
(Althaus); chloral hydrate alone, 4.0-6.0 ( 3 j- 3 jss.) a day, is 
uncertain in its action, but in combination with morphia often 
acts very well; antipyrine, which has lately been recommend- 
ed for all sorts of affections, may also be given a trial. The so- 
called revulsives (daily repeated cold-water enemata (Gussen- 
bauer), cold or warm poultices, sinapisms, superficial cauteriza- 
tion, the electric brush) often act splendidly where we want to 
produce temporary amelioration of the pain ; but, as we say, 



72 DISEASES OF THE CRANIAL NERVES. 

unfortunately this is only transient. The same is true of elec- 
tricity, which may be used according to the polar method 
(steady application of the anode over the painful place, cathode 
at some indifferent place, weak increasing - and decreasing cur- 
rents being used), or according to the method of direction of 
the current (descending steady current). Galvanism to the 
neck has also been advised. The constant current may be 
given atrial, combined with the action of chloroform, as Adam- 
kiewicz has proposed in his paper on cataphoresis. I have sev- 
eral times used the "diffusion electrode," which he recom- 
mends, quite successfully (cf. lit.). The faradic brush, the 
unpleasant action of which may be somewhat mitigated by 
putting moist blotting-paper on the skin, is often very satisfac- 
tory, and I can recommend the strong cutaneous faradization 
very highly even during the paroxysms. Operative inter- 
ference (neurectomy) has recently more and more, and justly 
so, fallen into disrepute. The results are often entirely nega- 
tive, and where some success has been obtained with it this did 
not prove lasting. Baths, especially at the non-medicated hot 
springs, a stay at the seaside or in the mountains, cold-water 
treatment, and vapor baths may be advised, but we are unable 
to state definitely which of these modes of treatment are indi- 
cated in any particular case. 

./Etiology. — About the astiology we know little worthy of 
mention. That heredity and exposure to cold have something 
to do with the disease we must admit ; but this is not peculiar 
to neuralgia of the fifth. However, anatomical changes (exos- 
toses, narrowing of bony canals due to syphilis, etc.) are here 
frequently of moment. Age, sex, occupation, do not seem to 
exert any particular influence ; still, the disease is on the whole 
very rare in small children, and if present it is always inherited. 

LITERATURE. 

Peyrounet de Lafonvielle. De la neuralgie du trijumeau et en particulier de 

son traitement par les pulverisations de la chlorure de methyle. These de 

Paris, 1886. 
Gussenbauer. Ueber Behandlung der Trigeminusneuralgie. Prag. med. Woch- 

enschr., xi, 31, 1886. 
Schech. Klonische Krampfe des weichen Gaumens mit objectivem Ohrgerausch 

in Folge von nasaler Trigeminusneuralgie. Miinchener med. Wochenschr., 

22, 1886. 
Adamkiewicz. Die Diffusionselektrode. Neurol. Centralbl , No. 18, 1886. 
Hirt. Breslauer arztl. Zeitschr., No. 22, 1886. 



THE DISEASES OF THE TRIGEMINAL NERVE. 



73 



Krieger. Centralbl. f. klin. Med., 44, 1886. (Antifebrine.) 

Seifert. Ueber Antifebnn als Nervinum. Wiener med. Wochenschr., 35, 
1887. 

2. Anesthesia of the Trigeminus — Paralysis of the Trigeminus. 

Paralysis of the sensory branches of the trigeminus is on 
the whole less frequently met with than neuralgia of the face. 
Only exceptionally are all the divisions (the motor portion of 
the third included) affected equally ; but most observations go 
to show that, as a rule, only individual branches suffer, and 
these not in their whole extent, but only within certain areas. 
The smaller the number of fibres in the distribution of which 
anaesthesia obtains, the more peripheral is the seat of the cause 
(Romberg), and we may assume an affection of one whole 
branch to exist " where the loss of sensation is found not only 
in certain areas of the surface, but also in the corresponding 
cavities of the face" (Romberg). Whether the branch is affect- 
ed before or after leaving the skull we have no means of de- 
ciding. 

A lesion of the first division also causes ansesthesia of the 
surface of the eyeball. Since, in consequence of this, influences 
from outside (foreign bodies, dust, traumatism) are not per- 
ceived, not infrequently a keratitis, which begins in the lower 
segment of the cornea, is developed. This may run into an 
inflammation of the whole ball and bring about destruction of 
the eye {ophthalmia paralytica). That to explain this condition 
we must not assume a lesion of special trophic nerves has been 
shown by experiments on animals (Senftleben). An affection 
of the second division deprives the nasal branches of their 
function, and the nose becomes not only insensible to external 
touch, but certain pungent smells — as, for instance, that of 
snuff — are no longer recognized on the affected side. In lesions 
of the third division the corresponding half of the tongue, but 
only in its anterior two thirds, loses its sensation, and the pa- 
tient has no longer any sense of taste in this area (n. lingualis) ; 
since, however, loss of taste in the anterior portion of the 
tongue has been observed in some cases where the function of 
the third division of the fifth was found to be perfect (Heus- 
ner), we can not exclude the supposition that the fibres of the 
chorda tympani (or at least a considerable part of them) join 
the facial from the second division of the fifth. Certain it is 
that the fibres which pass to the chorda return again to (the 



74 



DISEASES OF THE CRANIAL NERVES. 



second and third branch of; the trigeminus after having prob- 
ably run with the facial as far as the geniculate ganglion. 
From Fig. 13 the distribution of anaesthesia over the skin of 
the face may be learned. Vaso-motor changes, subjective sen- 
sations of heat and cold, sensations of being swollen, and dis- 
turbances in the movements of mastication, difficulty in open- 
ing the mouth (paresis of the external pterygoid and the ante- 
rior belly of the digastric), are sometimes met with (Miiller). 




Fig. 13.— Distribution of the Sensory Cutaneous Nerves on the Head. V lt F 2 , 
F 3 , the three branches of the trigeminus, «*, auriculotemporal. .», supraorbital.' st, 
supratrochlear, it, infratrochlear. /, lachrymal, m, mental. 3, buccinator, am, 
auricularis magnus. sm, subcutaneus mala, oma and omi, occipitalis major and mi- 
nor, cs, superficial cervical. 

The course of the disease depends upon the seat of the 
lesion. In peripheral affections the prospect for recovery is 
usually comparatively favorable; yet this is frequently only 
partial, and several of the qualities of sensation remain per- 
manently lost, the sensibility in general is dulled, and tactile 
paresthesias persist — in a word, recovery is imperfect. 

The treatment chiefly consists of excitants, among which 
the most efficient is the application of the faradic and the 
galvanic brush to the skin. Transient improvement may be 



THE DISEASES OF THE TRIGEMINAL NERVE. 



75 



thus obtained after a short while in the peripheral affections. 
This electric brush is the best excitant for the skin, and is to 
be preferred to all liniments and the like, which are supposed 
to act in much the same way. Internal treatment, provided 
there be no definite underlying disease, is absolutely super- 
fluous. 

LITERATURE. 

Miiller. Zwei Falle von Trigeminuslahmung. Arch. f. Psych, u. Nervenkrankh., 
xiv, 2, 3, 1883. 

Uthoff. Fall von Neuritis des rechten Trigeminus mit Affection des Lacrymalis 
und einseitigem Aufhoren der Thranensecretion. Deutsche med. Wochen- 
schr., xii, 19, 1886. 

Dana. A Case of Paralysis of the Trigeminus followed by Alternate Hemiplegia 
— its Relation tc the Nerve of Taste. Journ. of Ment. and Nerv. Diseases, 
xiii, 2, p. 65, 1886. 

Heusner. Eine Beobachtung iiber den Verlauf der Geschmacksnerven. Ber- 
liner klin. Wochenschr., xxiii, 44, 1886. 

Ferrier. Lancet, vol. i, No. 1, 1888. 

j, Trigeminal Cough. 

Finally, we may call attention to a reflex neurosis, which 
was first described by Schadewald, and then studied by VVille. 
This is a paroxysmal cough which, occurring in individuals 
whose respiratory organs are perfectly sound, is entirely due 
to an irritation of the trigeminal fibres distributed to the nose, 
pharynx, and the external auditory meatus. The just-men- 
tioned writers distinguish accordingly a nasal, a pharyngeal, 
and an auricular trigeminal cough, and declare the first (nasal) 
to be the most frequent variety. According to them also, this 
neurosis is by no means rare, and the possibility of its existence 
ought always to be thought of where we have to treat cases of 
an obstinate paroxysmal cough, which is liable to be produced 
by the action of pungent odors and by changes of temperature, 
and which is accompanied by hypersecretion of the nasal 
mucous membrane. The treatment consists in the use of the 
nasal douche, the application of weak induction currents di- 
rectly to the nasal cavity, and the administration of potassium 
iodide. Further observations are still needed to decide whether 
we actually have to deal in these cases with a neurosis of the 
trigeminus, or whether the vagus has not something to do 
with the affection, or whether finally, as Hack suggested, the 
erectile tissue of the nose is responsible for it. 

Quite lately it has been claimed that peripheral irritation of 



7 6 



DISEASES OF THE CRANIAL NERVES. 



the trigeminus (by inhalation of pungent vapors, new growths, 
etc.) may reflexly give rise to sensations of dizziness (" nasal ver- 
tigo," Joal). Until more confirmatory evidence is brought for- 
ward, it would be well to suspend judgment on this question. 

LITERATURE. 

Herzog. Der acute und chron. Nasencatarrh mit besonderer Berucksichtigung 
des nervosen Schnupfens ("Rhinitis vasomotoria"). 2. Aufl. Graz, 1886. 
Leuschner & Lubenski. 

Wille. Der Trigeminushusten. Deutsche med. Wochenschr., xi, 16, 17, 1885. 

Joal. Nasal Vertigo. Lancet, February 1, 1887, p. 31. 



CHAPTER V. 

DISEASES OF THE FACIAL NERVE. 

The facial nerve emerges at the base of the brain from the 
medulla oblongata by the side of the abducens and behind the tri- 
geminus on the posterior margin of the middle peduncle of the cere- 
bellum. The auditory nerve is situated close behind it, and between 
the two a separate bundle of fibres is placed — namely, a second root 
of the facial, the so-called nervus intermedius or portio intermedia 
Wrisbergii. With the auditory nerve the facial then passes for- 
ward and outward into the internal auditory meatus, at the bottom 
of which it enters through a small opening the Fallopian canal 
(cf. Fig. 16). In the hiatus of this canal it makes an almost rectan- 
gular turn (genu nervi facialis), passes backward and then down- 
ward, and leaves the skull through the stylo-mastoid foramen to 
divide inside of the parotid gland into the terminal branches, the 
temporo-facial and the cervico-facial, which form together the plexus 
anserinus major. At the so-called genu the nerve forms a gangli- 
form swelling — the ganglion geniculi — from which the larger super- 
ficial petrosal nerve is given off (cf. diagram, Fig. 16). These are 
the fibres which communicate with the trigeminus, and have the 
function of gustatory fibres for the anterior two thirds of the 
tongue (cf. page 73). 

The nucleus of the facial, a group of large multipolar ganglionic 
cells, lies four millimetres and a half beneath the floor of the fourth 
ventricle, in the region of the formatio reticularis, and above the 
upper olive (cf. Fig. 14). From this illustration it is also apparent 
that the ascending root of the trigeminus has the emerging portion 
of the facial root to its mesial side, while the anterior root of the 
auditory lies external to it. The axis cylinder processes of the gan- 
glionic cells of the nucleus are united in a larger fasciculus, forming 
the first part of the root (Ursprungsschenkel of Krause), which at 
the floor of the fourth ventricle becomes a compact bundle, the in- 
termediate portion (VII, a). At the anterior end of the eminentia 
teres this is bent at right angles (genu cerebrale), and becomes the 
emerging portion (Austrittsschenkel) of the facial (VII), which 



78 



DISEASES OF THE CRANIAL NERVES. 



reaches its point of exit, before mentioned, through the transverse 

fibres of the pons. 

Quite lately experiments on animals by Mendel have shown that 
n.VT Vila. m ra bbits and guinea- 

pigs the facial branches 
to the eyes take their 
origin in the oculo-mo- 
tor nucleus. Whether 
this is the case or not in 
man our present patho- 
logical observations do 
not allow us to decide 
with certainty. 




rur 



Fig. 14. — Diagram showing the Course of the Fa- 
cial Fibres in the Pons. (After Schwa lbe.) n. VII, 
facial nucleus. I'll b, root-bundle of the facial nucleus. 
VII a, intermediate portion (^cross-section). VII, emerg- 
ing; portion of the facial, n. VI, abducens nucleus. 
n. VIII, nucleus, and VIII, root of the auditory nerve. 
y, fibres coming from the raphe, x, fibres coming from 
the abducens nucleus, o. s., upper olive, a. V, ascend- 
ing root of the trigeminus. 

paralysis. We shall discuss each class 



Just as in the case 
of the trigeminus, so 
in the facial, we must 
distinguish between 
central (cortical and 
bulbar) and peripheral 
(intra- and extra-cra- 
nial) lesions, which, 
owing to the purely 
motor functions of the 
facial, may give us, 
clinically, spasm or 
separately. 



1. Facial Spasm — " Mimic Facial Spasm " — " Tic Convulsif." 

Lesions which give rise to facial spasm may be central or 
peripheral in their situation. In the first case either the cor- 
tex or the nucleus (or the root) of the nerve in the medulla 
oblongata is concerned. According to our present ideas the 
cortical area for the facial is located in the lower half of the 
anterior and the lower third of the posterior central convolu- 
tions, and it is also supposed that the posterior halves of the 
two lower frontal and the anterior part of the supramarginal 
convolutions have some, although a less important, connection 
with it (Exner). 

It is not known whether stimulation of these centres can 
produce a facial spasm, or, in other words, whether there exists 
a real cortical facial spasm. At least, we are unable to find 



DISEASES OF THE FACIAL NERVE. 



79 



anything in the literature to warrant such an assumption. The 
possibility that those cases of tic associated with involuntary 
explosions of obscene words, which have been reported by 
Gilles de la Tourette, Dana, and Wilkin, may be due to stimu- 
lation of the facial and speech centre in the cortex, is, perhaps, 
not to be excluded. It seems, however, well established that 
the disease can be produced by reflex stimulation of the facial 
nucleus (cf. the case of Berger and its treatment). Undoubt- 
edly, disease of the peripheral portions of the nerve is the most 
common, in which, just as in trigeminal affections, either the 
whole facial area or only individual branches may be affected. 
We distinguish a clonic and a tonic variety of spasm. 

A patient suffering from clonic diffuse facial spasm has lost 
control over his facial muscles, either on one or, more rarely, 
on both sides. The muscles affected are in irregular motion, 
so that against his will the patient makes the oddest faces, 
wrinkles his forehead, raises the alas nasi, screws his eyes up, 
etc. When the attack has passed he has a temporary respite, 
yet often enough the pause is very brief, and even during re- 
missions spasms flash across his face, so that his features are 
never for any time entirely at rest. On the slightest provoca- 
tion, by speaking, often also by eating, quite violent paroxysms 
are excited, so that the patient would fain cover up his dis- 
torted face. 

If the spasm is tonic, the affected side of the face is singu- 
larly rigid and takes no part in the facial movements, but is 
distorted. The muscles are distinctly hard to the touch, the 
corner of the mouth is pulled toward the diseased side, the 
mouth firmly closed, the eyebrow drawn up — signs sufficiently 
marked to distinguish it from facial paralysis, in which also the 
affected side does not take part in the movements of expres- 
sion. Vaso-motor and trophic changes are, as a rule, absent. 

In cases where the spasm is confined to some branches of 
the facial only, we find that the muscles around the eyes are 
almost always the ones affected. The eyelid is attacked by a 
clonic or tonic spasm, and conditions are developed which go 
under the names of spasmus nictitans and blepharospasm. 

The spasmus nictitans consists of spasmodic blinking, in 
which not only the eyes are rapidly closed and opened, but 
also the neighboring muscles (frontalis, zygomatici) participate 
in the spasmodic movements. In a mild form this spasm is seen 
in many people where it is only to be regarded as a bad habit. 



8o DISEASES OF THE CRANIAL NERVES. 

Blepharospasm consists of a paroxysmal spastic contraction 
of the orbicularis palpebrarum, lasting a few seconds or min- 
utes, which completely closes the lids. In rare cases the attacks 
follow each other so quickly and are so prolonged that the 
patient has to be treated as a blind man. The attacks appear 
unexpectedly and quick as lightning. They are often precipi- 
tated by voluntary firm closure of the eyes, eye-strain, or by 
the action of light, and the patient is utterly unable to raise the 
lid until the attack has passed. The physician, however, will 
succeed at times in cutting short the paroxysm if he be able to 
discover any of the so-called pressure points, which, according 
to von Graefe, who first discovered them, are often present. 
More or less firm pressure exerted at these points is capable of 
producing an interruption of the spasm and a cessation of the 
attack. Unfortunately, however, such points are often entirely 
absent, and when they exist their position is so uncertain and 
changeable that they may only be accidentally discovered. 
One of the few which is present with some constancy corre- 
sponds to the supra-orbital foramen. We should, however, 
look for them over the whole distribution of the trigeminus, 
over the spinous and transverse processes of the cervical verte- 
bras, and even in the region of the brachial plexus. It is our 
duty to make a frequent and untiring search for them, as we 
may thus be able to afford our patients very great relief. 

Course. — The course of the disease, be it in the form of a 
total or a partial spasm, is usually very tedious, and a progno- 
sis for recovery must be very guarded. The outlook is espe- 
cially unfavorable when the affection is complicated with other 
motor disturbances, as I have observed, for instance, in two 
cases where the facial spasm was associated with writer's 
cramp. Such complications, which are, according to my expe- 
rience, not common, render, as we said, the prognosis far more 
gloomy, and in such cases we must beware of too easily awak- 
ening hopes in the minds of our patients. 

^Etiology. — We know little about the aetiology of blepharo- 
spasm. That it may be of reflex origin can not be doubted. 
The most varied diseases of the eyes, affections of the trigem- 
inus, especially tic douloureux, carious teeth, intestinal worms, 
uterine troubles, may lie at the bottom of it, and the origin of 
the disease is cleared up only if, after removal of some primary 
cause, the spasm suddenly ceases. 

I saw a case of blepharospasm, which had persisted for 



DISEASES OF THE FACIAL NERVE. 8 1 

years and was considered hopeless, cured after a coexisting 
flexion of the uterus had been materially improved. Diseases 
of the blodcl-vessels can, furthermore, produce the spasm, as 
we see from the case of Buss (cf. lit.), where an atheromatous 
artery, and from that of F. Schultze, where an aneurism of the 
left vertebral artery by pressure upon the facial nerve brought 
on the spasm. Finally, hysterical conditions can lead to it, as 
is shown by the latest communications of Charcot on the so- 
called hemispasmus glosso-labialis, which has been described 
by Marie in the Progres med, (June 6, 1887). 

Treatment. — All these we must keep in mind in deciding 
upon a line of treatment, and not imagine that we can cure a 
facial spasm, whether it be total or partial, clonic or tonic, with 
indiscriminate galvanization, for without system we shall only 
meet with success in rare cases, and then only by good luck. 
The most promising plan of treatment is the application of the 
anode to pressure points if such be present, while the cathode 
is placed on some indifferent region, the back of the neck or 
the sternum. Weak currents applied for one or two minutes, 
with careful avoidance of make and break, give the best results. 
The application of the anode to the back of the head, keeping 
it at the same point, also sometimes meets with success (Berger), 
but too often leaves us in the lurch ; and this will hardly sur- 
prise us if we remember that even when the anode is placed on 
the back of the neck the abnormally stimulated reflex centre 
in the medulla is by no means always reached by those curves 
of the current which really do penetrate deeply. 

Cures, such as that reported by Berger, undoubtedly de- 
pend upon a happy coincidence of circumstances. The me- 
dulla oblongata, above all, where in such an astonishingly small 
space a number of the most important nuclei lie close together, 
seems to be the most unfavorable place for local electrization 
(Duchenne), by which we aim at affecting individual nerves or 
nerve roots. We may reach all or none, no matter whether we 
use small or large electrodes. Still, even this method ought to 
be tried, since we have no positive remedy. Should the gal- 
vanic treatment fail, the internal treatment is still more vague, 
and it is well to inform the patient of the uncertainty of this 
procedure. Of course, the usual nervines and antispasmodics 
are to be given. As a last resort, neurectomy of the supraorbi- 
tal or stretching of the facial nerve (Bernhardt, cf. lit.) has to be 
considered, yet even from this we can expect no lasting success. 
6 



82 DISEASES OF THE CRANIAL NERVES. 

LITERATURE. 

Berger. Neurolog. Centralbl., 10, 1883. | 

Bernhardt. Arch. f. Psych, und Nervenkrankh., xv, 3, 1884. 

Buss. Neurol. Centralbl., 14, 1886. 

Henschen. Reumatick tic convulsif med fbrtjocking af nervi facialis stam. Up- 

sala lakareforen fdrh. 1887, xxiii, 3. 
Guinon. Tics convulsifs et hysteric Revue de med., June, 1887. 
Cf. besides the text-books of Striimpell, Seeligmiiller, Eichhorst, Eulenburg, etc. 



2. Facial Paralysis— Mimic Facial Paralysis— Hemi- 
plegia Facialis — Prosopoplegia. 

Facial paralysis is an affection the relative frequency of 
which makes it of the greatest practical importance. In this 
more than in any other nervous disease any layman can easily 
judge just how much the art of the physician has accomplished 
in a certain time in a given 'case, and on this account it espe- 
cially behooves us at our first examination to be very careful 
in making a positive statement as to the prospects of recovery 
or the probable duration of the disease. Both these points de- 
pend chiefly on the seat of the lesion, which, as in tic convulsif, 
may be central or peripheral. 

A. CENTRAL FACIAL PARALYSIS. 

Symptoms and Diagnosis. — Central facial paralysis may be 
produced either by a cortical lesion (cortical paralysis) or by a 
lesion of the facial fibers in the brain between the cortex and 
the pons (intracerebral paralysis par excellence); or, finally, it 
may depend upon a disease of the nuclei and nerve roots in the 
pons. Cortical facial palsies may be caused by tumors, ab- 
scesses, or chronic inflammations in the region of the motor 
centres. Those of intracerebral origin may be produced by 
syphilitic arterial disease or by rupture of a vessel in the 
region of the internal capsule and the crus cerebri. The third 
form, that originating in the pons, is found in Duchenne's pa- 
ralysis and, more rarely, in tabes. Whether the facial paralysis, 
which appears and disappears in the course of hysteria is to be 
regarded as of central origin or not, can not be decided. 

The clinical picture differs but little in these three forms, 
and only at times do the accompanying symptoms make a dif- 
ferential diagnosis possible. Thus, for instance, the intracere- 
bral paralysis often appears with an apoplectic attack, and is 
accompanied by hemiplegia and speech disturbances, while if 



DISEASES OF THE FACIAL NERVE. 



83 



facial paralysis is found in connection with spinal disease it is 
always of nuclear origin. 

All three forms of central paralysis have usually, however, 
two features in common which can almost be regarded as 
pathognomonic and which distinguish them from the periph- 
eral paralysis, namely: 1. The presence of a normal electrical 
excitability in the nerves and muscles to both currents. 2. The 
escape of the upper facial branch. While in peripheral paraly- 
sis all three divisions are equally affected, we find in the cen- 
tral form the upper branch usually intact, and the patient can 
wrinkle his forehead and close both eyes. 

We say usually, not always, because there are undoubtedly 
exceptions, where we meet with a central paralysis in which the 
upper branch has not been spared. It is quite probable that 
the naso-labial and the orbiculo-frontal fibres of the facial have 
a separate cortical origin, and we can well imagine that if the 
cause of the paralysis — e. g., a small focus in the cerebrum — is 
situated above the union of those two branches, one remains 
intact (in the large majority of cases the upper), whereas if it is 
below their point of union both branches are affected. 

A further guide to localization is the condition of the move- 
ments of expression (Bechterew). If these are lost while the 
voluntary innervation of the facial muscles is intact, we have to 
assume a focus in the optic thalamus, the centre for facial ex- 
pressions, or close to it (Bechterew), while a facial paralysis 
with retained power of facial expression allows us to exclude a 
lesion in the thalamus and its coronal connection with the hemi- 
spheres. In the case of Rosenbach (Neurol. Centralblatt, 11, 
1886) there was an isolated paralysis of mimic expression in 
the left facial and right-sided bilateral hemianopia, and the 
lesion was taken to be in the right thalamus. 

In differentiating between a cortical and a bulbar facial pa- 
ralysis the following points must be taken into consideration : 
That the lesion is cortical is probable if the facial alone with- 
out the corresponding half of the body is paralyzed (mono- 
plegia facialis), and if the affection is confined to the lower 
branches of the nerve, while the normal reaction to the elec- 
trical current remains undisturbed. It is easy to understand 
that the hypoglossus often takes part in the lesion if we remem- 
ber in how close proximity the centres of the two nerves are 
situated in the cortex, and in a given case an examination of the 
mobility of the tongue will show whether we actually have to 



8 4 



DISEASES OF THE CRANIAL NERVES. 




deal with a so-called monoplegia facio-lingualis. Sometimes a 
disturbance of speech points at once to this combination. In 
every case in which we assume a cortical lesion, the sensation 
in the distribution of the facial and the hypoglossus ought to 
be tested, because it is just in these cases that we find not infre- 
quently sensory changes — e. g., analgesias and anaesthesias. Of 
these " cortical " sensory disturbances 
we shall speak further in the next part, 
where we shall discuss cortical lesions 
of the brain. 

We shall be led in a facial paralysis 
to think of an affection of the pons when 
not only the nerve, but with it one whole 
half of the body is paralyzed ; and there 
are two types of pontine facial paraly- 
sis according as the lesion is situated in 
the upper or lower part of the pons. In 
the first case (focus a in Fig. 15) the fa- 
cial and the same, in the second (focus 
b) the facial and the opposite half of the 
body are affected (hemiplegia alternans, 
Gubler, 1859), because the facial fibres 
cross in the pons and we may have a 
lesion above or below this crossing, and 
in both cases this will be situated, of 
course, above the crossing of the fibres 
going to the extremities (cf. also what is 
said further on about lesions of the 
pons). 

The facial paralysis caused by the 
lesion in the upper part of the pons, and 
that found in connection with hemi- 
plegia after a lesion in the internal cap- 
sule, are in so far alike as they are both 
accompanied by paralysis of the extremities on the same side. 
But there is one point of difference which will influence our diag- 
nosis, namely, that after pontine lesions the facial paralysis, very 
much as in the peripheral form, takes in all three branches of 
the nerve, while in a lesion of the capsule or the basal ganglia 
only the lower branches of the nerve are affected ; but in con- 
tradistinction to what happens in the peripheral paralysis the 
electrical condition may, at least in some cases, remain normal. 



Fig. 15.— Diagram showing 
the Decussation of the 
Fibres going to the 
Extremities, and of 
those going to the 
Face, in the Pons and 
Medulla Oblongata. E, 
facial fibres. E, fibres go- 
ing to the extremities. R, 
pons. O, medulla oblon- 
gata, pyx, decussation of 
the pyramidal tracts, a, a 
focus in the upper, b, a 
focus in the lower part of 
the pons (the latter is situ- 
ated below the decussation 
of the facial fibres'). 



DISEASES OF THE FACIAL NERVE. 85 

The most striking symptom of central facial paralysis is the 
relaxed and expressionless appearance of the affected side. 
The naso-labial fold is more or less distinctly flattened, the cor- 
ner of the mouth is slightly open and hangs down, the mouth 
seems to be drawn to the well side, the patient is unable to 
raise his upper lip or to whistle. On inflating the cheeks the 
air escapes ; drinking and speaking are difficult, the latter espe- 
cially, because the labial sounds are defectively formed. Dur- 
ing eating the food gets in between the cheek and the teeth on 
the affected side and the patient has to bring it to the right 
place again with the fingers. In biting, the mucous membrane 
of the cheek is often caught between the teeth. The upper 
part of the face is in by far the greater number of cases nor- 
mal ; the forehead can be wrinkled well in its whole extent, and 
the patient can frown and close either eye perfectly. 

The condition of the velum palati and the uvula varies, and 
is, therefore, of no value, either diagnostically or prognosti- 
cally. The uvula may deviate to the sound or to the affected 
side, or may occupy its normal position. With our still im- 
perfect knowledge of the innervation of the muscles concerned, 
any attempt to explain the different positions of the uvula must 
needs be hard, but we shall be less surprised at our difficulty 
when we consider that the levator palati is supplied not only 
by the facial through the large superficial petrosal, but very 
probably also by the vagus accessory, the tensor palati, how- 
ever, by the third branch of the fifth. In other words, at least 
three cranial nerves are concerned in the motion and fixation 
of the uvula, and besides, even under normal conditions, the 
uvula is occasionally found to deviate to one or the other side. 
The only thing of which we can, perhaps, be sure is that if 
during phonation paresis of the velum palati and deviation to 
the sound side becomes apparent, the large superficial petrosal 
is most likely affected (paralysis of the levator palati and azygos 
uvulae). Of greater importance for the diagnosis of central facial 
paralysis is the persistence of the reflexes, which in peripheral 
paralysis are often diminished or sometimes completely lost. 

Furthermore, the disturbances in hearing, the alterations 
in taste and in the salivary secretion, so frequently observed 
in the latter, are almost always absent in central affections. 

The existence of a bilateral facial paralysis — diplegia facialis 
— points as a rule to a central lesion, and more especially to a 
bulbar affection. It certainly is one of the greatest rarities to 



86 DISEASES OF THE CRANIAL NERVES. 

have a simultaneous paralysis of both as the result of a pe- 
ripheral lesion. 

Prognosis. — The prognosis depends upon the anatomical 
basis of the disease. Lesions of the cortex and the pons often 
bring about facial paralyses that are incurable, while those ob- 
served in conjunction with capsular hemiplegias, especially in 
the early stages of the latter, frequently present a decided im- 
provement after a time. 

Treatment. — The question of treatment arises only when 
the primary lesion is amenable to therapeutic measures. Since 
this, however, is only very rarely the case, it is best, at least in 
the central facial paralysis, to restrict ourselves to the expect- 
ant treatment. The measures that will be recommended as in- 
dicated in the peripheral form are here of very little avail. 

B. PERIPHERAL FACIAL PARALYSIS. 

In its peripheral course the facial may be divided into two 
portions — an intracranial and an extracranial. The former 
is less frequently affected than the latter, which is more ex- 
posed to atmospheric influences, especially cold. For prac- 
tical reasons we prefer to consider the diseases of these two 
segments separately. 

/. The Intracranial Lesion. 

This form is distinguished by the fact that besides the con- 
stant existence of paralysis of all the facial branches, we have 
often certain concomitant symptoms, which can only be fully 
understood if we picture to ourselves the exact course of the 
nerve. This can be done with the help of the diagram (taken 
from Erb) here represented, which permits an accurate locali- 
zation of any given intracranial lesion. 

(a) If the lesion be between the exit of the facial stem (from 
the pons) and the geniculate ganglion, we shall find a paralysis 
of the velum palati, abnormal acuteness of hearing, and dimin- 
ished salivary secretion. 

(6) If the facial be affected in the region of the geniculate 
ganglion itself, then we find in addition to the just-mentioned 
symptoms alterations in the sense of taste. 

(c) A lesion between the geniculate ganglion and the stape- 
dius nerve produces the symptoms described in a and b, but no 
abnormality of the velum palati. 

id) A lesion between the origin of the nerve to the stape- 



DISEASES OF THE FACIAL NERVE. 



87 



dius muscle and the giving off of the chorda tympani gives 
alterations in the sense of taste and diminished salivary secre- 
tion, but no abnormality of hearing or of the velum palati. 

(e) It, finally, the nerve is diseased below the giving off of 
the chorda, in the Fallopian canal, we only find paralysis in the 
distribution of the posterior auricular branch without any 
trouble with taste, hearing, the condition of the velum palati, 
or the secretion of saliva. We should state again, however, 
that in all cases from a to e all the facial branches take part in 
the paralysis. 

Valuable as this diagram is, undoubtedly, regarded from a 
theoretical stand-point, yet in practice we but rarely meet with 
opportunities for observing cases which exactly correspond to 
it ; nevertheless, in every instance we should not fail to attempt 
to locate the lesion with as much accuracy as possible. 

A physiological explanation for the appearance of the above- 
mentioned concomitant symptoms is not always easy. That 
alterations in the sense of taste are due to lesions of the chorda 
tympani can not be doubted, and if they are present the lesion 
is situated between the geniculate ganglion and the giving off 
of the chorda ; if they are absent the lesion must be sought 
below this region. The disturbance in the sense of taste is 
limited to the anterior two thirds of the tongue, and exists, of 
course, only on the paralyzed side. Sensory changes in the 
tongue are not necessarily present. Less clear is the cause of 
the diminished salivary secretion. Its occurrence is said to 
point to a lesion above the geniculate ganglion (Wachsmuth). 

Among the most common and best known symptoms are the 
disturbances in hearing, which consist either in an abnormal 
acuteness of hearing (hyperacusis, oxyacoia) or in a decrease 
in the power of hearing. In the first case, where we have a 
kind of hyperaesthesia for all musical tones, the alteration is 
supposed to be due to a paralysis of the stapedius muscle (which 
is supplied by the facial) and a consequent overaction of the 
tensor tympani (Lucae, Hitzig, Roux). The latter — the hard- 
ness of hearing — can be due to several causes. We may either 
have a disease of the middle ear and the adjoining portion of 
the temporal bone, which has affected the facial nerve by con- 
tiguity, or a simultaneous affection of the auditory nerve, which, 
in the internal auditory meatus, has been exposed to the same 
deleterious influence, and become affected by the same disease 
as the facial. Quite lately again the frequency of this combina- 



88 



DISEASES OF THE CRANIAL NERVES. 



tion of facial paralysis with a slight paralysis of the auditory 
nerve has been pointed out by O. Rosenbach (cf. lit.). 




Fig. 16.— Erb's Diagram for Facial Paralysis. Representing the course of the facial 
trunk from the base of the skull to the pes anserinus. N. a., auditory nerve. N.f., fa- 
cial nerve. N. p. s. , large superficial petrosal nerve. G. g. , geniculate ganglion. N. c. c.p. t., 
communicating branch to tympanic plexus. JV.st., stapedius nerve. Ch. t., chorda 
tympani. G./., gustatory fibres. Sps., secretory nerve to salivary glands. F.st., stylo- 
mastoid foramen. N. a. p., posterior auricular nerve. 



2. The Extracranial Lesion. 

The peripheral paralysis of the facial after its exit from the 
skull is, as we have already said, the most common. Of this 



DISEASES OF THE FACIAL NERVE. 89 

class the so-called rheumatic form, which is attributed to the 
influence of cold (a frigore), and the traumatic, often observed 
after operations, gunshot injuries, etc., are the two chief repre- 
sentatives. When any one, heated as he is, passes from a warm 
room into a cold wintry night, or is exposed to drafts in the 
railroad cars, and finds himself a few hours later taken with a 
paralysis of one side of the face, this is the so-called rheumatic 
form which has attacked the stem of the nerve after its exit 
from the Fallopian canal. In these cases all three facial branches 
are affected, and the appearance of the patient is changed in a 
very material and striking manner. Even the layman notices 
that he now wrinkles only one half of his forehead, and that the 
folds and furrows generally present are obliterated on one side ; 
that the patient can shut one eye only while the other remains 
wide open and can not be closed despite the strongest efforts. 
If the attempt is made, the eyelids remain gaping, the eyeball 
is rolled inward and upward, and the pupil disappears behind 
the upper lid, a position which is also maintained during sleep 
(lagophthalmos). The inability to shut the lids prevents the 
tears from running into the tear ducts and interferes with the 
process by which foreign bodies, particles of dust and the like, 
are removed from the eye. It happens, then, that the tears are 
always running down the cheeks, and that a conjunctivitis, even 
an ulceration of the cornea, may be developed through the 
mechanical irritation caused by such foreign bodies. The ap- 
pearance of the lower part ol the face has already been de- 
scribed 

Concomitant symptoms, such as we have found in intra- 
cranial lesions, are in these cases, as a rule, absent. The patient 
complains of nothing else than of his inability to move the facial 
muscles as he wishes and the (secondary) trouble with his eyes. 
Speech and mastication are interfered with to a marked degree 
only in severe cases. It has been mentioned already that the 
reflexes are decreased or lost. 

A complication which, though not frequent, is of great in- 
terest when met with in peripheral facial paralysis, namely, 
herpes zoster, has been lately described by Letulle, Striibing, 
and Voigt (cf. lit.). Whether this is due to an inflammation 
of the peripheral endings of the fifth, which is transmitted to 
the facial (Striibing), or whether the stem of the facial contains 
in parts fibres, an inflammatory irritation of which may pro- 
duce herpes zoster (Eulenburg), is not clear. 



9 o 



DISEASES OF THE CRANIAL NERVES. 



I have only in rare instances seen this complication, and 
have found that whenever it was present the cases pursued an 
unusually protracted course. 

When a relapse occurs, as happens sometimes, but, after 
all, rarely, the course, is equally unfavorable, according to my 
own observation. Mobius has reported such instances (cf. 
lit.), but his experience as to recovery seems to have been 
less unfavorable than my own. In one of my cases there inter- 
vened between the second and first attack eight years. In the 
first one the cure was effected after four weeks ; in the second 
not until six and a half months had passed. 

The instances of the facial paralysis, which repeatedly at- 
tacks the same individual, form an interesting counterpart to 
the cases where several members of the same family suffer 
repeatedly from the disease, cases such as Neumann has re- 
ported from Charcot's polyclinic of the Salpetriere (Du role de 
la predisposition nerveuse dans l'etiologie de la paralysie faci- 
ale dite a f rigor e. Arch, de neurologie, July, 1887, x i v > 4°)- It 
seems as if the influence of cold, etc., only forms the immediate 
exciting cause for the disease, and that this would probably 
not appear unless the patient were burdened with some he- 
reditary tendency — i. e., came from a neuropathic family 
(Charcot). 

Duration and Course. — The duration and course of rheu- 
matic facial paralysis are extremely variable, and it is of great 
importance for the physician to be able to give at the begin- 
ning an approximately accurate opinion as to the length of time 
necessary for recovery. This we can, however, only do if we 
investigate the electrical condition of the paralyzed muscles, 
and hence it follows that it should be our invariable rule to 
make an electrical examination before venturing upon any ex- 
pression of opinion. The following are the chief points to 
guide us : 

1. If we find no changes either in faradic or in galvanic ex- 
citability the prognosis is favorable ; recovery in from seven to 
twenty days (light form). 

2. If we find the faradic and galvanic excitability of the 
nerve diminished, but not lost, the galvanic excitability of the 
muscles, however, increased, and the usual formula of contrac- 
tions changed (A. C. C. > C. C. C), then the prognosis is rela- 
tively favorable ; recovery in from four to six weeks (interme- 
diate form of Erb). 



DISEASES OF THE FACIAL NERVE. 9 1 

3. If the reaction of degeneration be found — i. e., if the far- 
adic and galvanic excitability of the nerve and the faradic ex- 
citability of the muscles be lost, while there is an increase in the 
galvanic excitability of the muscles associated with qualitative 
changes and changes in the mechanical excitability — then the 
prognosis is relatively unfavorable, and for recovery two, four, 
six, eight, even twelve months, may be required (grave form). 
These are those bad cases in which secondary contractures 
and spasmodic twitchings of the muscles also appear, which, 
according to Hitzig's opinion, are to be referred to an obscure 
abnormal irritation in the medulla oblongata. It is well to 
know that, as convalescence begins, voluntary motion may re- 
turn long before the electrical excitability, so that often the 
patient is able to perform some slight voluntary movements be- 
fore faradic stimulation provokes the least contraction. 

Diagnosis. — With regard to the diagnosis there is even for 
the beginner no more easily recognizable disease. Still there 
are cases where it is difficult, not to say whether there is any 
paralysis, but, strange as it may sound, which is the affected 
side. One is particularly liable to mistakes in old people, in 
whom the wrinkled, inelastic skin has produced a stereotyped 
expression, which, even when the facial muscles contract, is 
but little changed. Suppose now the muscles to have lost their 
innervation, the paralyzed side takes on the soft features of an 
earlier period of life, and this may go so far that the patient 
believes his rigid, wrinkled side to be the paralyzed, and the 
affected side the healthy one (Gowers). We also must remem- 
ber that the non-paralyzed zygomatici pull the face sharply 
toward the well side, a condition which easily produces in the 
layman the impression of something abnormal, so that he takes 
the side thus distorted for the diseased one. In general, how- 
ever, we may say that the diagnosis of a peripheral facial paral- 
ysis is one of the easiest imaginable in neuropathology. 

Treatment. — In the treatment we may in recent cases rec- 
ommend for trial steam-baths and counter-irritation to the skin ; 
but never, unless there is a special indication, should internal 
remedies be advised, because in a non-complicated rheumatic 
facial paralysis they are absolutely superfluous. In more pro- 
tracted cases the methodical use of electricity is strongly indi- 
cated, for even though it is undoubtedly true that the disease, 
if the prognosis is at all favorable, gets well of its own accord, 
and really requires no treatment at all, there can, on the other 



9 2 



DISEASES OF THE CRANIAL NERVES. 



hand, be no doubt but that the electrical treatment hastens the 
cure in a marked degree ; therefore, electricity should be used 
under all circumstances. Just which method should be em- 
ployed can not be definitely laid down, but we should keep in 
mind that not only the galvanic current is beneficial, but that 
the faradic brush applied to the stem and the individual 
branches of the facial gives good results, and the patient 
should, therefore, be persuaded to submit to this somewhat 



Lower branch of 
the facial. 



Region of the cen- 
tral convolutions. 



Facial stem. 
Middle branch of the facial. 




Supraclavicular 

point (plex. 

\ brach.). 



Fig. 17.— Some of the so-called "Motor Points" on the Face and Neck. 



disagreeable procedure. The places from which the most 
important facial muscles can best be stimulated are seen in Fig. 
17. At these points the motor-nerve branches to the muscles 
concerned lie very near the surface. They are called " motor 
points " (Ziemssen). In galvanization every specialist has his 
pet method of application and his own ideas about the strength 
and direction of the current. The one prefers to apply the 
electrode over the mastoid process, placing either the anode or 
the cathode on the affected side of the face ; another treats at 



DISEASES OF THE FACIAL NERVE. 



93 



the same time the sympathetic in the neck ; a third, again, ap- 
plies the anode over the affected nerve and the cathode to an 
indifferent point, and so forth. Whichever method we may 
prefer, the main thing-, after all, is to produce by repeated 
opening and closing of the current contractions of the mus- 
cles by which the tonus of the latter will soon be improved. 
I should like to mention, too, that I have seen the application 
of the galvanic brush and the use of the combined current (de 
Wattewille) repeatedly attended with satisfactory results. 

LITERATURE. 

Romberg. Op. cit., pp. 349 et seq. 

Erb. Arch. f. klin. Med., v, 5 and 6, p. 518, 1869. 

Huguenin. Schweizer Correspondenzbl, 7, 8, 9, 1872. 

Letulle. Arch, de Physiol., 2me ser., ix, p. 662, 1882. 

Eulenburg. Ueber Complicationen von peripherer Facialislahmung mit Zoster 

faciei. Centralbl f. Nervenheilk., 5, 1885. 
Voigt. Petersburger med. Wochenschr., ix, 45, 1885. 
Remak. Centralbl. f. Nervenheilk., 5, 1885. 

Remak. Sitzungsbericht d. med. Gesellsch. zu Berlin vom 22. April 1885. Ber- 
liner klin. Wochenschr., 22, 1885. 
Gilles de la Tourette. Arch, de Neurol., ix, p. 19, 1885. 
Strubing. Deutsches Arch. f. klin. Med., xxxvii, p. 513, 1885. 
Mobius. Schmidt's Jahrb., Bd. 207, p. 249, 1885. 
Mobius. Centralbl. f. Nervenheilk., ix, 7, 1885. 
Uargaud. De l'hemiplegie faciale dans la periode secondaire de la syphilis. 

These de Paris, No. 178, 1885. 
Dana and Wilkin. Journ. of Mental and Nerv. Diseases, No. 7, 1886. 
Gowers. Op. cit., p. no, 1886. 
Sinkler. Med. News, September 25, 1886. 
Grancher. Gaz. med. de Paris, p. 47, 1886. 
Marie. Progres med., 6, 7, 1887. 
Brieger. Charite-Annalen, xii, p. 150, 1887. 
Rosenbach, O. Centralbl. f. Nervenheilk., x, No. 12, 1887. 
Neumann. Archives de neurol., xiv, 40, July, 1887. 
Eichhorst. Handbuch der speciellen Pathologie und Therapie, Bd. Hi, 3. Aufl. 

Wien, 1887. 
Chisolm. Arch. f. Augenheilk., xvii, 4, p. 414, 1887. (Congenital Paralysis of 

the Sixth and Seventh Pair of Cranial Nerves.) 
Mendel. Ueber den Kernursprung des Augenfacialis. Neurol. Centralbl., No. 

23, 1887. 
Huet. Hysterische Facialisparalyse. Weekblad v. d. Nederl. Tijdschr. v. 

Geneesk., 25, 1887. 



CHAPTER VI. 

DISEASES OF THE AUDITORY NERVE. 

The auditory nerve emerges at the base of the brain, alongside 
of the facial, and takes with this latter a forward and outward course. 
After having entered the internal auditory meatus, it divides before 
reaching the cribriform plate, which separates the internal meatus 
from the internal ear, into two main branches, an anterior inferior 
and a posterior superior. These nerves pass as small filaments 
through the openings in the plate, to be distributed respectively to 
the cochlea and vestibule, and are hence called ramus cochlearis and 
ramus vestibularis. 

The cortical centre of the nerve is probably to be sought for in 
the temporal lobe; the fibres are said to run through the last third 
of the posterior division of the internal capsule, through the middle 
geniculate body, through the brachia conjunctiva posteriora, the 
posterior corpora quadrigemina, and the inferior fillet (v. Mpnakow, 
Baginsky). 

About the situation of the nuclei of the auditory nerve there 
seems still to exist a difference of opinion among the anatomists. 
Usually two nuclei are distinguished, an inner or principal nucleus 
and an outer one situated laterally from the first. In their structure 
these present material differences. While the former — the inner 
nucleus — only contains scattered, small, slender, ganglionic cells (15 
to 20 ix long), the latter contains cells of considerable size (60 to 100 
\i long and 15 to 21/i broad). The situation of the two nuclei may 
be understood from the accompanying diagram. 

Of the two roots, the superficial terminates in the internal audi- 
tory nucleus, while the deeper one passes between the restiform body 
and the ascending root of the fifth, and turns toward the outer one. 
This, also, the diagram, which is taken from Wernicke, and which 
demonstrates the views of Meynert, illustrates. 

Although the diseases of the auditory nerve are not, as a 
rule, treated of in neurological text-books, they are found some- 
times so closely connected with other nervous diseases, and 



DISEASES OF THE AUDITORY NERVE. 



95 



are, notwithstanding their comparative rarity, of such decided 
practical importance, that we feel not only justified but com- 
pelled to consider them here, at least briefly. 

The nerve, as we have said, rarely ever becomes primarily 
diseased, but diseases of the middle and internal ear— that is, 
peripheral affections— are by far the most common causes of 




Fig. 18.— Diagrammatic Section through the Medulla Oblongata in the Region 
of the (Lower) Olive. The right half represents a lower plane, p, pyramids ; ot, 
lower olive ; /, lemniscus ; mf, motor region of the tegmentum ; 5, ascending root of the 
fifth; ci., corp. restif.; 8. e., external, 8. z'., internal nucleus of the auditory ; et., emin. 
teres; 12, nucleus and root of the hypoglossus ; 10, root of the vagus; X.a., anterior, 
X. p., posterior vagus nucleus ; X./., combined root of the " lateral mixed system " (cf. 
p. 105) ; 8. s., superficial, 8, p., deep root of the auditory nerve. 

diminution or loss of hearing. We may distinguish between 
conditions of irritation and those of paralysis, so that on the 
one hand we shall have hyperesthesias, on the other pareses 
or paralyses. 



I. Hyperesthesias of the Auditory Nerve. 

We speak of a hyperesthesia of the auditory nerve where 
the patient experiences a painful sensation in his ear when per- 
ceiving certain sounds or noises. For instance, in excitable 
and nervous individuals who suffer from hemicrania or tic 
douloureux, such a sensation may be produced by high musical 



g5 DISEASES OF THE CRANIAL NERVES. 

notes, whistling, and the like. Quite a different affection is an 
abnormal acuteness of hearing, which is extremely rare, the so- 
called oxyacoia of which we have spoken in the chapter on 
facial paralysis. 

Frequently one hears nervous patients complaining of sub- 
jective auditory perceptions, roaring, buzzing, hissing, singing, 
humming, and the so-called nervous tinnitus aurium, which 
may persist during the whole life without a sign of any other 
disturbances of function. This symptom may be due to a 
purely functional disorder or it may be the forerunner of a 
middle-ear sclerosis. 

Therapeutically, we may, after the removal of masses of 
cerumen or epidermis which may have obstructed the outer 
canal, with benefit make use of blisters, stimulating lotions ap- 
plied to the mastoid process, subcutaneous injections of mor- 
phine, the bromides, digitalis, and atropine. If abnormalities 
of tension in the sound-conducting apparatus and consequent 
rise of pressure in the labyrinth be the cause of the disorder, 
then the inflation of the middle ear and the rarefaction of the 
air in the outer canal is to be recommended. 

II. The Pareses and Paralyses of the Auditory Nerve. 

Analogous to the rheumatic facial paralysis we have a con- 
dition in the auditory nerve which manifests itself in either a 
decrease or a loss of the function of hearing, the so-called rheu- 
matic acusticus paralysis. It is less frequent than the former, 
although the cause of both, namely, cold, is the same. Central 
paralyses are always connected with decrease of hearing power 
on one side only. Absolute unilateral deafness, as a conse- 
quence of a focal lesion in one of the hemispheres, has up till 
now not been observed (Wernicke). Whether the disturbances 
in hearing observed by Baginsky in railway spine are of a cen- 
tral or peripheral nature remains yet to be studied (cf. lit.). 

Next in order we have to mention in this connection the 
anaesthesia and paresis of the auditory nerve, which sometimes 
appear quite suddenly in the course of hysteria, and often as 
suddenly disappear again after a longer or shorter period of 
time. We shall consider these forms more carefully in the 
chapter on hysteria. 

Of interest from a pathological standpoint is the nervous 
deafness occurring after an epidemic cerebro-spinal meningitis. 
It is this form which has been so thoroughly studied by Moos. 



DISEASES OF THE AUDITORY NERVE. 



97 



There is hardly any doubt but that it is caused by the passage 
of purulent masses from the meninges along the sheath of the 
auditory nerve into the inner ear. The prognosis is unfavor- 
able. A diminution of hearing, probably due to transitory cir- 
culatory disturbances, occurs sometimes after epileptic attacks. 
Although not common, this affection is certainly well authen- 
ticated. 

Of especial interest getiologically are the disorders of hear- 
ing which we find in engineers and firemen on the railroads as 
a consequence of their occupation. This must principally be 
attributed to the noise, aided, however, to some extent by the 
abrupt and severe changes of temperature and the exposure to 
all kinds of weather. We do not know anything positive about 
the relative frequency of this affection, which consists in a more 
or less pronounced decrease of hearing, but in the general in- 
terest of the public it certainly deserves as much attention on 
the part of the companies as the color-blindness which has for 
years been carefully looked into. Locksmiths, blacksmiths, 
and boiler-makers, whose auditory nerves are also being con- 
stantly overstimulated, suffer from similar disorders. In rare 
and exceptional cases it has been observed that mechanics who 
are " hard of hearing " hear better during the usual noise con- 
nected with their work than when everything around them is 
quiet — paracusis Willisii. This very remarkable phenomenon 
is probably due to a decrease in the vibratory power of the 
auditory ossicles, owing to which the sound is conducted with 
more difficulty, a condition which is obviated by a more forci- 
ble concussion (Buerkner, Roosa). We would not leave un- 
mentioned the fact that an overtaxation of the auditory nerves 
lasting for years causes great nervousness, and may even pre- 
dispose to mental diseases. 

In the treatment, endermic inunctions of strychnine (o.i to 
glycerin io.o (gr. jss. ; glycerin, 3 ijss.) — sig., ten drops) over 
the mastoid process, and fumes of sulphuric ether conducted by 
a catheter into the tympanic cavity to act on the distribution of 
the acusticus, deserve recommendation. A beneficial effect 
from the galvanic current can be expected only if examination 
assures us that the current has a modifying influence on the 
subjective noises or upon the power of hearing. This treat- 
ment necessitates a knowledge of the investigations of Brenner 
on the galvanic reactions of the auditory nerve (cf. Erb, Hand- 
buch der Elektrotherapie, 1882, page 226). 
, 7 



qS DISEASES OF THE CRANIAL NERVES. 

III. Meniere's Disease — Meniere's Vertigo— Vertigo ab 

AURE L.ESA — VERTIGO IN GENERAL. 

When we speak of Meniere's disease we mean a combina- 
tion of symptoms which is made up (i) of subjective noises in 
the ear, (2) a feeling of dizziness, accompanied with vomiting, 
(3) a gradually increasing difficulty of hearing, sometimes end- 
ing in deafness. 

On account of the exceptionally practical importance which 
has to be attributed to the so-called vertigo {le vertige, Schwin- 
delgefiihl), we may be allowed to make some general remarks on 
this before considering the special form, viz., Meniere's disease. 

By vertigo we mean a subjective feeling of motion appearing 
suddenly or gradually without any loss of consciousness, at- 
tended by a simultaneous sensation of loss of equilibrium. The 
subjective sense of motion is either referred to the body or parts 
of it, or to surrounding objects. The motion is in different 
directions, sometimes in horizontal or vertical circles, revolving 
with their convexity sometimes forward, sometimes backward, 
and the older observers distinguish accordingly a vertigo titu- 
bans, fluctuans, etc., from the nutatio — that is, subjective move- 
ments in a straight line. As concomitant symptoms we note 
headache, especially in the back of the head, anxiety, tremor, 
cold sweat on the face, nausea, vomiting ; in grave cases, 
transient loss of consciousness, as in the prodromal state of an 
apoplectic attack. If consciousness is completely retained, as 
happens in the majority of cases, the subjective sensation of 
movement often gives rise to objective voluntary movements, 
to be regarded in a measure as instinctive efforts against the 
threatening danger of falling. The patient plants his feet firm- 
ly on the ground, stretches out his arms into the air, seizes 
with his hand any object within his reach, etc., but, in spite of 
all, he may, notwithstanding the perfect retention of conscious- 
ness, fall, owing to the feeling of disturbed equilibrium — ver- 
tigo caduca. 

If the patient is unconscious — e. g., asleep — then he experi- 
ences a sensation of falling down from a great height, down 
steps, out of the window ; he imagines himself sinking into an 
opening in the ground, etc. This so-called nocturnal vertigo 
{Traumschwindel) usually torments those who suffer from ver- 
tigo when awake. Two exquisite examples of this vertigo I 
have observed in Bright's disease. 



DISEASES OF THE AUDITORY NERVE. QQ 

By far most commonly the vertigo occurs in paroxysms 
which appear without regularity and are of variable duration. 
Between the first and second sometimes hours and days, more 
rarely months, and indeed whole years, intervene, and only 
exceptionally — e. g., in cerebellar affections — do the subjective 
sensations of movement persist uninterruptedly, and thus render 
the vertigo constant. 

The position of the body has rarely any influence on the 
vertigo, for although at times some amelioration is felt on sit- 
ting down, there are cases in which the vertigo continues even 
when the patient occupies the horizontal position in bed. The 
pathogenesis of the trouble — that is to say, the organic changes 
in the brain which are necessary for the production of the sen- 
sation — are but little understood. It is generally supposed 
that changes in the blood-pressure, due, perhaps, to stimulation 
or paralysis of the vaso-motor nerves, are the chief cause of 
vertigo, just as a lasting decrease or increase in the amount of 
blood in the brain can probably give rise to attacks of dizziness. 
Until the conditions under which vertigo can appear in other- 
wise healthy people are more accurately understood, our 
knowledge of the pathological influences at work can be only 
imperfect. Of great interest are the experiments of Purkinje, 
undertaken sixty years ago, as to the influence of swinging, and 
especially of circular movements, in the production of vertigo, 
These were published in Rust's Magazin fur die gesammte 
Heilkunde, part 23, 1827, and have been reprinted in Rom- 
berg's Nervenkrankheiten (Joe. cit., p. 118) with this addition by 
the author : " From all these experiments we see that, taking 
the head as a sphere, around the axis of which the true motion 
takes place, an imaginary plane through it determines in every 
case the apparent motion of the objects in the subsequent 
position of the head at rest. The same holds good in attacks 
of vertigo." 

Johannes Miiller also has made experiments on vertigo, and 
is inclined to attribute it to the after-effects of visual impressions 
on the retina. That this, however, is not always the case is 
shown by the fact that vertigo may appear in people whose 
eyes are closed, and even in the blind. 

We have already spoken about its occurrence in the paral- 
ysis of the ocular muscles (p. 45). Here let us add that this 
ocular or visual vertigo disappears if the patient closes the 
affected eye or holds his head in such a position that the 



IQ o DISEASES OF THE CRANIAL NERVES. 

paralyzed muscle does not come into play during the act of 
seeing. 

In the present chapter we shall discuss more especially how 
far diseases of the internal and middle ear are connected with 
vertigo. It has repeatedly been observed that affections of the 
nasal mucous membrane, swellings of the erectile tissue, have 
produced it. If, then, we add that it has been claimed that the 
intestines (intestinal worms, taenia, ascaris) and the stomach 
are responsible for feelings of dizziness, which Trousseau calls 
"vertigo a stomacho Iceso" we can not fail to be impressed with 
the complexity and the lack of clearness in the aetiology of 
this affection. We must, however, always keep in mind, no 
matter where the remote cause lies, be it in the faulty move- 
ments of the ocular muscles, in the nose, in the ears, or in the 
stomach, etc., we must keep in mind, I say, that the influence 
of the cerebrum and the cerebellum is under all circumstances 
quite essential for the production of vertigo. Whether the 
characteristics of the vertigo vary or not with the different 
organs affected is not yet clearly known. 

The disease described by Gerlier in Ferney, which shows itself by 
a very pronounced dizzy feeling, appearing in paroxysms — the so- 
called "paralyzing vertigo" — is accompanied by other symptoms, 
namely, a weakness, resembling a paralysis, in the extremities, droop- 
ing of the eyelids, and extraordinary lassitude without any loss of 
consciousness. This condition, which has been repeatedly observed 
in the canton of Geneva, where it occurs epidemically among labor- 
ers and herdsmen, is aetiologically mysterious. Gerlier attributes it 
to miasmata from marshes and stables, but this does not explain the 
immunity of the female sex. For this new and as yet entirely 
strange neurosis Gerlier has proposed the name vertige paralysant 
(Progres m^d., 1887, 26; Deutsche med. Zeitung, 1887, 44, 1888, 24). 

Middle life and moderately advanced age (especially in the 
female sex, and so in them the climacteric period) seem to pre- 
dispose to attacks of vertigo, which chooses by preference its 
victims from among vigorous and full-blooded individuals. Its 
frequent occurrence in advanced old age will not surprise us if 
we remember the atheromatous condition of the arterial walls 
and the consequent irregularities of the blood supply to the 
brain substance. Among the exciting causes, unaccustomed 
circular rocking movements, such as we feel on board ship, 
play an important role — it is interesting that children possess a 



DISEASES OF THE AUDITORY NERVE. IO I 

wonderful immunity (sucklings rarely or never become sea- 
sick) — prolonged stooping, straining at stool, an overloaded 
stomach, can give rise to vertigo. The dizziness experienced 
on looking down from a height — the " height dizziness " — which 
has erroneously been attributed to a fear of danger, is probably 
a reflex movement evoked by a wrong conception of our posi- 
tion in space, the result of a purely optical illusion ; for its pro- 
duction not only the cerebrum and cerebellum, but also the 
action of the retina is needed. 

The prognosis in vertigo depends upon the nature of the 
primary disease, and Boerhaave's expression, " vertigo est om- 
nium morborum capitis levissimus et facillime curabilis," has 
to be taken cum grano salts. In an organic lesion of the cere- 
bellum — that is, of the vermiform process — we can expect no 
improvement in the vertigo, while if it is attributable to an 
anaemia of the brain, occurring as a symptom of a general 
anaemia, the outlook is decidedly favorable. 

In the same way the treatment will be different in different 
cases according to the primary disease, which always has to 
be taken into consideration. For the symptomatic or prophy- 
lactic treatment, the repeated administration of mild laxatives, 
the frequent use of strong stimuli to the skin, such as cold 
douches, brushing of the neck and the back, mustard plasters, 
regular bodily exercise, and well-regulated diet, are to be rec- 
ommended, while any overloading of the stomach, especially 
in the evening, should be strenuously avoided. In spite of the 
much-lauded remedies (cocaine, etc.) we do not possess any 
reliable medicinal treatment for sea-sickness and height diz- 



After this digression we will return to the consideration of 
that form of vertigo which is especially connected with aural 
disturbances. Notwithstanding the fact that it is by no means 
settled that the above-mentioned combination of symptoms 
constituting Meniere's disease can be produced by a pure neu- 
rosis of the auditory nerve, we will take it up here, because 
under all circumstances this nerve plays a prominent part in 
the pathology of the affection. 

Since Meniere in 1861 first described the disease, it has been 
repeatedly observed and carefully studied by German physi- 
cians. All have, however, failed as yet to give us a clear un- 
derstanding of its pathology. Meniere himself believed that 



102 DISEASES OF THE CRANIAL NERVES. 

an extravasation of blood or an acute exudation takes place 
into the labyrinth, which produces the same symptoms as oc- 
cur in animals after injury to the semicircular canals. This 
view is in so far incorrect in that cerebral affections, accumula- 
tions of cerumen, and diseases of the middle ear, can undoubt- 
edly produce the same symptoms ; and then we have to re- 
member that not the haemorrhage nor the exudation, but its 
action upon certain parts of the membranous labyrinth is neces- 
sary before the symptoms occur (Politzer). It can easily be 
imagined that whenever the extravasation stimulates the nerves 
of the ampullae Meniere's symptoms are produced, while they 
are absent if the haemorrhage does not directly press upon the 
nerves of the antrum or the ampullae (Politzer). 

Quite recently Brunner (cf. lit.) has put forward a supposi- 
tion which we think is worth considering, namely, that we may 
be dealing with a vaso-motor neurosis of the vessels of the laby- 
rinth. According to him the pressure in the labyrinth acts in 
a similar way as pressure in the cranial cavity, where con- 
siderable changes are borne as long as the normal expansion 
of the subdural and subarachnoid space is not interfered with. 
He thinks, therefore, that narrowings of the labyrinth could 
produce a predisposition to Meniere's disease. 

This hypothesis is extremely plausible, especially as the 
symptoms appear paroxysmally, and in the intervals the patient 
is apparently in perfect health. In this way also the favorable 
action of quinine can be explained if we suppose that it dimin- 
ishes the hyperaemia in the semicircular canals, just as Horner 
has shown to be the case for the retinal vessels. He observed 
that large doses of quinine constantly produced considerable 
ischaemia in the latter. The question is, however, not settled, 
and we have to confine ourselves for the present to a most 
careful study of the clinical manifestations of the disease. 

There are hardly two cases in which the symptoms are ex- 
actly the same, and the course is so far from being uniform 
that we can not be surprised if often great uncertainty about 
the diagnosis prevails. The onset even is very variable. Now 
it is sudden with loss of consciousness and apoplectiform symp- 
toms, etc. ; again it is gradual, first, subjective noises in the 
ears being noticed, sometimes comparable to the whistle of a 
locomotive, sometimes to the rustling of the leaves in the forest. 
Next comes a feeling of dizziness, at times only moderate, at 
times so pronounced that the patient in spite of all his efforts 



DISEASES OF THE AUDITORY NERVE. 



103 



falls to the ground. Vomiting may be present or absent. 
Finally, a decrease in the power of hearing, first in one, then 
in the other ear, becomes noticeable. Some cases show a de- 
cided progressive tendency. After short remissions the symp- 
toms always reappear with increased severity, the vertigo 
gains so much in intensity that now the patient repeatedly falls 
with great violence, vomiting becomes more and more fre- 
quent, and the patient becomes at first incapable of following 
his calling, and finally is reduced to the state of a useless mem- 
ber of society. In rare instances periods of marked improve- 
ment, which may indeed last for years, occur. In these even 
the difficulty in hearing may be gradually diminished, and the 
prognosis becomes relatively favorable. Finally, it is at times 
observed that with the full development of the deafness all the 
other symptoms, buzzing in the ears, vertigo, and vomiting, 
disappear. In other words, we have what we call a relative 
recovery or recovery with defect. In any given case we are 
never in a position to predict the outcome, and have always to 
be very guarded in our prognosis. 

Of considerable diagnostic importance is the fact that usu- 
ally the examination of the drum and the Eustachian tube does 
not reveal any changes, and that neither cranial nor spinal 
nerves present any disturbances of function. Rinne's test 
gives variable results in Meniere's disease. This test consists, 
as is well known, in applying a vibrating tuning-fork with 
moderate pressure first over the mastoid process, leaving it 
there until the patient seems to hear the sound, and then as 
quickly as possible bringing it immediately in front of the ex- 
ternal meatus, avoiding all contact with the head or ear. If 
the patient then is able to hear the sound of the tuning-fork 
once more, this is a sign that, as is normally the case, the con- 
duction through the air is better than through the bone. If, 
on the other hand, he does not hear it, the conduction through 
the air must in some way be interfered with. In the diagnosis 
these are points to be considered. 

In the treatment, above all, the action of large doses of 
quinine — 0.7-1.0 (gr. x-xv) pro die — must be tried, a procedure 
warmly recommended by Charcot, and later used with gratify- 
ing results by Fere, Moos, and others. In many cases, as we 
have said, the effect is very marked and there is no need to seek 
further for other medication. At times, however, this will fail, 
and then we are forced to resort to a two-per-cent solution of 



io4 



DISEASES OE THE CRANIAL NERVES. 



pilocarpine (nine to ten drops subcutaneously), a drug which is 
supposed to favor absorption. The result is often surprising. 
I have seen grave symptoms completely subside after three or 
four days' use of this medicine. The injections are to be con- 
tinued every second day for three or four weeks, and, as a rule, 
after the fifteenth dose the treatment can be discontinued, at 
any rate for a time. We need not add that on administering 
this drug the general condition of the patient must be carefully 
looked after, and any symptoms of collapse guarded against by 
the timely exhibition of stimulants, wine, and the like. 

LITERATURE. 

Moos. Ueber Meningitis cerebrospinalis epidemica, insbesondere iiber die nach 

derselben zuriickbleibenden combinirten Gehors- u. Gleichgewichtsstorun- 

gen. Heidelberg, 1881. 
Moos. Erkrankungen des Gehororganes bei Locomotivfuhrern und Heizern. 

Zeitschr. f. Ohrenheilk., x, 4, 1881 ; xi, 2, 1882. 
Gottstein u. Kayser. . Breslauer arztl. Zeitschr., iii, 18, 1881. 
Biirkner. Arch. f. Ohrenheilk., xvii, 1, 2, p. 8, 1881. 
Jacoby. Ibid., xvii, 4, p. 258, 1881. 

Burckhardt-Merian. Schweizer Correspondenzbl., xiv, 1, 6, 1884. 
Roosa. Zeitschr. f. Ohrenheilk., xiii, 2, 3, 1884. 
Finkelstein. Wratsch, No. 1, 1886. 
Baginsky. Ueber Ohrerkrankungen bei Railway-spine. Berliner klin. Woch- 

enschr., 3, 1888. 

Meniere's Disease. 

Charcot. Klinische Vortrage iiber Krankheiten des Nervensystems. Deutsch 
von Fetzer, Abthlg. ii, p. 343. Stuttgart, 1878. 

Guye. Arch. f. Ohrenheilk., xvi, 1, 2, 1880. 

Fere and Damars. Revue de med., i, 10, 1881. 

Woakes, Edward. Remarks on Vertigo and the Group of Symptoms some- 
times called " Meniere's Disease." Brit. Med. Journ., April 28, 1883, p. 801. 

Bechterew. Neurol. Centralbl., 9, 1887 (anatomical study on the origin of the 
auditory nerve). 

Brunner. Zum Morbus Meniere. Zeitschr. f. Ohrenheilk., xvii, 1, 2, p. 47, 
1887. 

Politzer. Lehrbuch der Ohrenheilkunde. 2. Aufl., p. 488 et sea. Stuttgart, 
1887. 

Striimpell. Op. cit., p. 420 et sea., 1887. 



CHAPTER VII. 

DISEASES OF THE GLOSSO-PH ARYNGEAL NERVE. 

The glossopharyngeal nerve leaves the brain between the root 
fibres of the auditory and those of the vagus, at the side of the 
medulla oblongata, by five or six filaments ; these soon unite to form 
an anterior (small) and a posterior (larger) bundle ; they both pass 
outward, under and in front of the flocculus, to the anterior division 
of the jugular foramen, through which the nerve leaves the skull. 
Whether the so-called jugular ganglion which the nerve presents 
while still inside the skull has to be looked upon as a special gan- 
glion or only as a group of nerve-cells which have separated them- 
selves from the petrous ganglion, which is seen on the nerve immedi- 
ately after its exit from the skull, remains to be decided. 

The glosso-pharyngeal has no nucleus of its own, but originates 
in a large collection of nerve cells, which are regarded as the nucleus 
common to this nerve, the vagus, and the accessorius. This nucleus 
is situated midway between the anterior and posterior spinal roots. 
In the manner in which its root fibres originate it corresponds partly 
to the motor, partly to the sensory type (Wernicke). It is therefore 
designated as the mixed lateral system (Deiters), and it is supposed 
that the glosso-pharyngeal originates in the upper, the vagus in the 
middle, and the accessory in the inferior portion of the nucleus (cf. 
Fig. 18, p. 95). The manner in which this common nucleus is com- 
posed is not yet understood, nor do we know how many modes of 
origin for root fibres of this "lateral mixed system" we have to as- 
sume. Exact data may be found in Wernicke's text-book, i, p. 155 
et seq. 

The glosso-pharyngeal, which, according to our present 
ideas, has to be regarded as the only genuine nerve of taste, is 
the third one which is to be taken into consideration in the 
examination of the functions of taste. The trigeminus (the 
third branch (lingual), possibly also the second branch) and the 
facial (chorda tympani) we have treated of, and it remains, 
therefore, to determine whether and if so under what condi- 



io 6 DISEASES OF THE CRANIAL NERVES. 

tions diseases confined to the glosso-pharyngeal occur, and in 
what manner taste is altered by them. Since it only supplies 
the posterior third of the tongue with sensory fibres (ramus 
lingualis nervi glosso-pharyngei), it is not to be wondered at 
that, in determining an isolated affection of the nerve, we not 
rarely meet with considerable difficulties. 

We know but little about central diseases of this nerve. It 
is supposed, however, that there exists a bulbar affection, a 
gray degeneration of the nucleus which is found in tabes (Er- 
ben), also that the gustatory paths may be in a state of irrita- 
tion which gives rise to alterations in taste-perception analogous 
to the paresthesias which occur with irritation of the paths of 
tactile sense in the posterior columns of the cord. Conduction 
anaesthesias are also said to occur, although it is impossible to 
decide whether only the glosso-pharyngeal or whether in ad- 
dition the trigeminal and the facial paths are concerned (cf. 
Fr'ankel, Berl. klin. Wochenschr., No. 3, 1875). A central 
paralysis of taste manifesting itself solely on the posterior third 
of the tongue has never been observed. With the cortical 
centre of the glosso-pharyngeal we are not as yet acquainted. 

Peripheral anaesthesia, anaesthesia gustatoria, ageusia (a, 
priv., yevo-is, sense of taste), impairment or loss of taste pro- 
duced by affections of the peripheral nerve endings, has been 
met with in diseases of the mucous membrane of the tongue, 
and has been known to be produced by the action of low tem- 
peratures (ice) or acrid substances (vinegar, chewing tobacco, 
red pepper). In testing for such alterations the patient is asked 
to close his eyes, open his mouth widely, and protrude his 
tongue ; then a small portion of sugar or quinine, etc., is placed 
upon that part of the tongue the function of which is to be 
tested, and the patient is to indicate with his finger where he 
perceives the taste before he retracts his tongue, and tell us by 
signs what he has tasted. The test is made with bitter, sour, 
sweet, and salty substances, and for the purpose any one, as 
long as it is not poisonous, may be selected. Further, it is pos- 
sible to accurately determine the boundaries of the area with 
normal and that with disturbed function of the tongue by means 
of the galvanic current. As we know, a sour, metallic, the 
so-called galvanic taste is perceived if the electrode is placed 
upon the tongue and the current is closed ; the same taste is 
experienced during galvanization of the throat, the neck, or 
head, and is probably produced by the current acting upon the 



DISEASES OF THE GLOSSO-PHARYNGEAL NERVE. 



107 



taste nerves in their peripheral or central course. The use of 
the galvanic current is also to be recommended in the treat- 
ment of the affections of the nerve. 

LITERATURE. 

Romberg. Op. cit., pp. 148 et seq. 

Erb. Handbuch 4er Krankheiten des Nervensystems, pp. 219 et seq., 1876. 
Heusner. Eine Beobachtung liber den Verlauf der Geschmacksnerven. Ber- 
liner klin. Wochenschr., No. 44, 1886. 



CHAPTER VIII. 

DISEASES OF THE VAGUS (PNEUMOG ASTRIC NERVE), " VAGUS 
NEUROSES." 

Immediately behind the superficial origin of the glosso-pharyn- 
geal on the postero-lateral aspect of the medulla oblongata, the vagus 
appears, with its ten to fifteen separate bundles, which soon unite to 
form one trunk. This is a fiat band which, accompanied by a process 
of the dura, passes outward below the flocculus, together with the 
accessorius, to the anterior division of the jugular foramen, inside of 
which is to be found the ganglion of the root of the vagus, or, as it 
is also called, the jugular ganglion. After its exit from the skull 
the vagus receives a part of the accessorius, and forms the gangli- 
form plexus or the ganglion of the trunk, which, however, only trans- 
mits a part of its fibres. 

About the difference in the further course of the left and right 
vagus we shall have a few words to say later. 

That the nucleus of the vagus is only a part of the nucleus com- 
mon to it, the glosso-pharyngeal, and the accessorius, has already 
been stated in the preceding chapter. The cells of the part belonging 
properly to the vagus are spindle-shaped, multipolar, 30 to 45 jx. long 
and 12 to 15 jx broad (hence much smaller than the cells of the hypo- 
glossus nucleus, which we shall describe later). As another impor- 
tant origin of the root fibres of the vagus, a compact round nerve 
bundle following the longitudinal axis of the medulla oblongata must 
be mentioned. It has been described by Meynert as the solitary fas- 
ciculus, while Krause designates it as the respiratory fasciculus, be- 
cause it connects the vagus with the origin of the most important 
respiratory muscles (cf. Fig. 19). The so-called nucleus ambiguus (in 
the diagram n. am) is held to be still another nucleus of the vagus. 
This is a collection of peculiar nerve cells situated within the forma- 
tio reticularis to the mesial side of the nucleus lateralis. 

Just as most of the cranial nerves, the vagus may be dis- 
eased in its centre as well as in its peripheral course. The 
first class of cases are usually met with as partial manifesta- 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). 



IOQ 



tions of other, general, diseases (tabes, hysteria). The latter 
are distinct affections in themselves, which may occasionally 
be due to peripheral causes, such as indigestion, catching cold, 
or reflex influences, diseases of the intestines and the uterus. 
Very frequently, it is true, the seat of the disease remains ante 
as well as post mortem obscure, and this is not to be won- 
dered at if we remember that mXf nam. 
we know little or nothing 
about the pathological anato- 
my of the vagus. Among the 
cases hitherto observed, many 
were not fitted to throw any 
light on the symptoms mani- 
fested during life, as in nu- 
merous instances no abnor- 
mality at all was found in the 
nerve, so that we are led to 
assume that the disease was 
purely functional (i. e., a dis- 
ease without appreciable ana- 
tomical basis). The pathol- 
ogy of the vagus, therefore, 
belongs to the most obscure 
chapters in the pathology of Fi s- 19— cross-section through the me- 
dulla Oblongata. (After Schwalbe.) 
a. V, ascending root of the fifth. n.XII, 
nucleus of the hypoglossus. n.X and n.X' , 
nucleus of the vagus. XII, hypoglossal 
nerve. fs, solitary funiculus (respiratory 
fasciculus), p, pyramidal tract, o, olive. 
i. N, pyramidal nucleus. /.La., anterior lon- 
gitudinal fissure. n.a?n, nucleus ambiguus. 
n. /., nucleus lateralis. 




the cranial nerves, and the 
following can only be consid- 
ered to be an imperfect at- 
tempt at giving a compre- 
hensive exposition of the high- 
ly interesting diseases con- 
nected with this nerve. 

Since the symptoms may sometimes be the same whether 
the disease is of central or peripheral origin, we shall, so as to 
avoid repetition, deviate from our usual method of division, and 
give our attention chiefly to the question how lesions of the 
vagus may influence (a) respiration, {b) circulation, (c) digestion, 
functions which, as is well known, are chiefly under the con- 
trol of this nerve ; next, we shall take up the consideration of 
exophthalmic goitre, an affection which possibly ought to be 
classed among the vagus neuroses. 



HO DISEASES OF THE CRANIAL NERVES. 

A. Affections of the Air-passages due to Lesions of 
the Vagus. 

i. The larynx, above all, interests us in this connection. This 
organ is innervated by the vagus and the accessorius, though it is 
still a matter of doubt whether all the motor fibres originate from 
the latter or only those that innervate the muscles used in the pro- 
duction of voice, while the vagus presides over the respiratory move- 
ments of the vocal cords ; the sensory fibres of the larynx certainly 
all belong to the vagus. 

The branches of the vagus, which come off in the cervical portion 
of the nerve and innervate the laryngeal muscles, are the superior 
laryngeal and the inferior or recurrent laryngeal. The former leaves 
the vagus at the lower end of the gangliform plexus, and divides into 
a motor branch, which goes to the crico-thyroid muscle, and into a 
sensory branch, which contains the fibres for the mucous membrane 
of the epiglottis and the whole laryngeal mucous membrane above 
the vocal cords. 

The recurrent laryngeal is shorter on the right side, because, with- 
out going beyond the upper aperture of the thorax, it curls around 
the subclavian artery, and runs back in a groove between the trachea 
and the oesophagus upward to the larynx, while on the left side it has 
to make the long course around the arch of the aorta. Its terminal 
branch (R. terminalis) divides into two twigs, which together supply 
all the muscles of the larynx, with the exception of the above-men- 
tioned crico-thyroid, with motor nerves, and the mucous membrane of 
the parts below the vocal cords with sensory fibres. 

Of the laryngeal muscles, the posterior crico-arytenoids draw the 
vocal cords apart — that is, they are the abductors or openers — while 
the lateral crico-arytenoids in conjunction with the lateral thyro- 
arytenoids draw them together, and are therefore called adductors or 
closers. Of these muscles, on each side the " abductor " arises at the 
posterior surface of the cricoid cartilage and passes upward and out- 
ward to the end of the muscular process of the arytenoid cartilage, 
while the other, the " adductor," arises from the upper margin of 
the cricoid cartilage and is inserted at the outer side of the muscular 
process of the arytenoid cartilage. It moves the muscular process 
forward, being thus the antagonist of the abductor. The crico- 
thyroids provide for the elongation and tension of the vocal cords ; 
they are assisted by the internal thyro-arytenoids, which run parallel 
with the vocal cords. 

In the laryngeal muscles paralysis and, though compara- 
tively rarely, spasms have been observed. 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). IIZ 

The chief forms of paralysis, which we shall here consider, 
are (i) the paralysis of the recurrent laryngeal, in which case 
all the muscles supplied by this nerve are paralyzed (or weak- 
ened) ; (2) the so-called abductor paralysis — that is, paralysis of 
the posterior crico-arytenoids, the openers of the glottis ; (3) 
paralysis of the internal thyro-arytenoids. 

Without going into the much-discussed and still unsettled 
question as to the mechanism of these paralyses, we have at- 
tempted to give a succinct and clear summary of the clinical 
symptoms, including the appearances found on laryngoscopical 
examination (cf. table on page 1 14). 

The existence of a cerebral centre for the laryngeal muscles 
is shown by the fact that in different cerebral affections — e. g.., 
pseudo-bulbar paralysis and certain brain tumors — paresis or 
paralysis of the vocal cords has been observed. In chorea ad- 
ductor paresis has been noted. A most curiously perverted 
action of the vocal cords has been observed by Krause in the 
course of hysteria ; on inspiration they were approached, while 
on expiration the glottis was wide and gaping. 

Another form of central paralysis is the nuclear. In com- 
plete paralysis of one vocal cord a lesion in the accessorius 
nucleus of the corresponding side has been found ; the usual 
cause of this, however, seems to be a peripheral affection of the 
trunk of the vagus, or of the recurrent laryngeal (by pressure, 
contusion, injuries, surgical operations, tumors, and aneurisms), 
yet we are not often in a position to speak with certainty as to 
the seat of the affection, and to say whether this is central or 
peripheral. The nature of the laryngeal paralyses which occur 
in general neuroses (hysteria, epilepsy), intoxications (lead), in- 
fectious diseases (diphtheria, dysentery, cholera), is quite ob- 
scure. The easiest to understand are those acquired through 
straining of the voice and diseases of the larynx itself (catarrh, 
perichondritis). (B. Frankel on mogiphonia, cf. lit.) 

The prognosis ought to be guided by the consideration of 
the nature of the primary affection, but we should also take into 
consideration the functions of the affected muscles, and not 
forget that, for instance, in abductor paralysis, danger of suffo- 
cation may arise at any moment. It is always unwise to pre- 
dict the exact time of recovery ; the course of such paralyses 
is usually very protracted. 

The treatment of most of the cases has to be conducted by 
a specialist, and consists in touching the vocal cords with the 



H2 DISEASES OF THE CRANIAL NERVES. 

sound (Rossbach), and in the external or intralaryngeal use of 
electricity. Faradization of the different laryngeal muscles 
necessitates a dexterity which can only be attained after a thor- 
ough acquaintance with the laryngoscopical technique. The 
general treatment of any primary affection need not be dis- 
cussed here. 

Spasms of the laryngeal muscles, we have said before, are 
very rare, and are in general, with the exception of the spasm 
of the glottis, of not much practical importance. Most fre- 
quently the spasm affects the adductors, and the condition then 
resembles very much that of abductor paralysis, with this excep- 
tion, that the spasm is generally quite transitory, while the paral- 
ysis is often of long duration. The aphonia spastica described 
by Schnitzler, a disturbance of co-ordination of the muscles of 
the vocal cords, which, on an attempt at phonation, contract 
spasmodically, is found occasionally in chorea and hysteria. 

The spasm of the adductors, which occurs especially in 
early childhood, is called spasm of the glottis (laryngismus 
stridulus, laryngospasmus, asthma thymicum sive Millari). Its 
paroxysms usually occur unexpectedly without external cause. 
They consist in the main in a total arrest of respiration lasting 
from several seconds to a minute and a half, and are ushered in 
by a deep inspiration which is accompanied by signs of suffo- 
cation. Only rarely does the child die during the attack ; 
usually a few deep, very audible respirations indicate the cessa- 
tion of the spasm, and the child seems completely well after a 
comparatively short while. No definite statement can be made 
with regard to the number and intensity of the individual at- 
tacks, because innumerable variations can occur. The anatom- 
ical seat of the disease is entirely unknown ; yet the fact that 
not rarely eclampsia or epilepsy complicates the affection rather 
speaks for the possibility of a temporary irritation of the corti- 
cal centre for the laryngeal muscles. The remarkably frequent 
occurrence of it in conjunction with rachitis has led to the idea 
(Elsasser) that we are dealing with a rachitic softening of the 
posterior part of the skull, which has rendered possible pressure 
upon the brain. Nothing definite is known about the cause. 
In the treatment early hardening of the child and rational 
nutrition play an important role. Robust, well - nourished 
children who can stand changes in temperature without at 
once catching cold, etc., are hardly ever affected with laryngis- 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE), i^ 

raus stridulus ; only delicate children with a convulsive tend- 
ency, who have been fed on farinaceous foods and other inap- 
propriate substitutes for the mother's milk, fall a prey to the 
disease. There is no medicinal treatment for the affection. 
During the attacks we have to avoid the danger of suffocation 
by carefully watching the epiglottis, sprinkling the body with 
ice-water, brushing and tickling the soles of the feet. After 
the attack we may give nervines (belladonna, bromide) and, 
perhaps to avoid a too frequent repetition, narcotics (morphine, 
i to 3 milligrammes — gr. V^- 1 /^ subcutaneously). The treatment 
of the rachitis should never be omitted. 

Sensory disturbances of the larynx manifest themselves 
either in anaesthesias, or, what is less common, in hyperesthe- 
sias of the mucous membrane, and are especially found in the 
distribution of the superior laryngeal. They are not rarely 
combined with motor changes, paralysis or paresis of the pha- 
ryngeal muscles (cf. chapter xi), but often they appear alone. 
The most common form is the anaesthesia attending diphthe- 
ritic paralysis ; it is characterized by the absence of the re- 
flex gagging and cough which normally follow touching the 
laryngeal mucous membrane with the sound, the finger, or the 
laryngoscope. In such cases it may happen that the food on 
deglutition enters the larynx, and, through faulty closure of 
the glottis, can not be removed by coughing, and thus gives 
rise to dangerous attacks of choking, and even to aspiration 
pneumonia. The latter does not seem to occur in cases of 
purely hysterical anaesthesia. 

The hyperaesthesia is found in ulcerative processes, or in 
bad, acute catarrhs. Although it seems to play a prominent 
role in hysterical patients, it is in reality not present, but is 
either simulated or erroneously said to exist by patients who 
are forever worrying themselves and finding out new ailments. 

The anaesthesia calls for electrical treatment, galvanization 
of the larynx and the palatal muscles, the faradic brush to the 
throat, etc. To meet the hyperaesthesia, narcotic remedies may 
be of service, but in hysterical patients often no other treat- 
ment but a good sensible lecture is needed. 

LITERATURE. 

Lazar. Ueber doppelseitige Lahmung der Glottiserweiterer. Diss, inaug., 

Breslau, 1879. 
Omerod. Paralysis of the Recurrent Laryngeal. Lancet, i, March n, 1880, i. 



114 



DISEASES OF THE CRANIAL NERVES. 



TABLE OF THE MOST COMMON PARALYSES OF THE LARYN- 
GEAL MUSCLES. 





Kind of 
paralysis. 


Occurrence. 


Symptoms. 


Ophthalmoscopic picture. 




Complete 


In compression 


Voice not clear. 


Vocal cords slightly ab- 




recurrent 


paralyses of the 


Patient is easily 


ducted, the so-called 




laryngeal 


vagus or the re- 


tired on talking. 


" cadaveric position " 




palsy. 


current laryngeal 


Coughing impos- 


(Fig. 20). In forcible 






(carcinoma oeso- 


sible. 


phonation the healthy 






phagi), often uni- 




cord reaches beyond 






lateral (left), as 




the middle line. Over- 






initial symptom of 




riding of the arytenoid 






aortic aneurism. 




cartilages (Figs. 21, 22). 






In tabes. 








Abductor 


In diseases of the 


If bilateral: extreme 


Glottis appears as a nar- 




paralysis 


nerve itself, the 


inspiratory dysp- 


row slit, becoming still 


< 


(paralysis of 


causes of which 


noea; if unilateral: 


narrower on inspira- 


o 


the posterior 


are often un- 


inspiration ham- 


tion (Fig. 23). In- 


> 


crico- 


known. 


pered.long-drawn, 


ability to abduct the 


Pi 

< 

H 
2 


arytenoids). 




noisy. Dyspnoea 


paralyzed vocal cord 






on the least ex- 


(Fig. 24). 






ertion. Speech 




O 






but little affected. 




u 
w 

PS 


Paralysis of 


In catarrhs of the 


Voice hoarse; speak- 


Glottis does not close 


the internal 


mucous mem- 


ing an effort. 


completely on phona- 


o 


thyro- 


brane of the lar- 




tion (Fig. 25). If at 


o 


arytenoids. 


ynx. After over- 




the same time the aryt- 


s 




exertion of the 




enoids are paralyzed, 


(X, 




voice. In hys- 




the glottis presents an 






teria. 




hour-glass outline (Fig. 
26). Neither anterior 
nor posterior portion is 
closed, but the vocal 
processes are in their 
normal position. 




Adductor 


Rarely isolated. In 


Absolute absence of 


Nothing characteristic. 




paralysis 


hysteria. 


voice. Power of 






(paralysis of 




coughing retained. 






the lateral 




" Phonic paraly- 






crico- 




sis" (Ttirck). 






arytenoids). 








*3 

O w 


Paralysis of 


After diphtheria. 


Voice rough ; high 


Excavation of the vocal 


H* 


the crico- 




tones impossible. 


cords. Cords do not 




thyroids. 






vibrate visibly. 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). 115 





Fig. 20. — Bilateral Paralysis of the 
Recurrent Laryngeal. " Cadaveric 
position " of the vocal cords. 



Fig. 21.— Recurrent Laryngeal Paraly- 
sis. Overriding of the arytenoid car- 
tilages. 





Fig. 22.— Paralysis of the Recur- 
rent Laryngeal on the Left Side 
(in inspiration). 



Fig. 23.— Paralysis of both Posterior 
Crico-arytenoids (in inspiration). 





Fig. 24.— Paralysis of the Right Post. 
Crico-arytenoid (in inspiration). 



Fig. 25. — Paralysis of both Internal 
Thyro-arytenoids (acute laryngitis). 




Fig. 26.— Paralysis of both Internal Thyro-arytenoids, 

associated with paresis of the arytenoid muscle. 
Figs. 20-26.— Partly after Strumpell, partly after Eichhorst. 



U6 DISEASES OF THE CRANIAL NERVES. 

Rosenbach, O. Ueber einen Fall von doppelseitiger Stimmbandlahmung. 
Breslauer arztl. Zeitschr., i, 2, 3, 1880. 

Hayes. Dubl. Journal, 3 S., lxix, p. 34, January, 1880. 

Rosenbach, O. Monatsschrift f. Ohrenheilk., etc., No. 3, 1882. 

Schech. Zur J£X\o\. der Kehlkopflahmungen. Ibid., No. 8, 1883. 

Dehio. Petersburger med. Wochenschr., 22, 1883. 

Aysaguer. L'Union, 46, 1885. (Bilateral Abductor Paralysis during Preg- 
nancy. Two Tracheotomies. Recovery.) 

Baumler. Deutsches Arch. f. klin. Med., Bd. xxxvii, Heft 4, 5, 1885. (Recur- 
rens Paralysis after Inhalation of Dust.) 

Gerhardt. Stimmbandlahmung und Icterus. Deutsche med. Wochenschr., No. 
16, 1887. 

Wegener. Ueber Kehlkopfmuskellahmung als Symptom der Tabes. Inaug. 
Dissert. Berlin, 1887. 

Frankel, Bernh. Ueber die Beschaftigungsschwache der Stimme, Mogiphonie. 
Deutsche med Wochenschr., 1887. 

Holmes, Gordon. Paralysis of the, Abductors of the Vocal Bands. Lancet, Oc- 
tober 22, 1887. 

Kidd. Bilateral Paralysis of the Dilator Muscles of the Glottis, with subsequent 
Paresis of the Constrictors. Lancet, July 16, 1887, p. 108. 

Kussner. Zur Kenntniss der Vagus-Symptome bei der Tabes dorsal. Berliner 
klin. Wochenschr., No. 20, 1887. 

Ziemssen, v. Ueber diphtheritische Lahmung und deren Behandlung. Klin. 
Vortrage, iv, Leipzig, Vogel, 1887. 

Eisenlohr. Zur Pathologie der centralen Kehlkopflahmungen. Arch. f. Psych, 
und Nervenkr., xix, 2, 314, 1888. 

2. The lungs receive from the thoracic portion of the vagus the 
pulmonary or bronchial nerves, the so-called anterior branches of 
which, in conjunction with filaments of the sympathetic, form a plexus 
on the anterior wall of the bronchus, and enter with the latter the 
lungs, while the posterior branches, together with those coming from 
the four upper thoracic ganglia of the sympathetic, are distributed 
in the same way on the posterior surface of the bronchus. They 
are the motor nerves for the unstriped muscles of the bronchial tree. 

The diseases of the bronchial nerves, which produce, as 
it seems, a faulty innervation of the circular muscles of the 
bronchi, give rise to the morbid condition which has lately 
been the subject of much controversy, and is described under 
the name 

Bronchial Asthma, Asthma Bronchiale s. Convulsivum s. Nervo- 
sum, Spasmus Bronchialis {Romberg). 

Pathology. — Opinions about the nature of bronchial asthma 
are still divided. While some (Stork, Frantzel) maintain that 
it is due to an acute swelling- of the bronchial mucous mem- 



DISEASES OF THE VAGUS {PNEUMOGASTRIC NERVE). Xl j 

brane, others (Bamberger, Wintrich) consider a tonic spasm of 
the diaphragm to be responsible for it ; still others (Trousseau, 
Biermer) believe it to be a vagus neurosis, supposing, in conse- 
quence of a disturbed innervation (vagus), a tonic spasm to take 
place in the circular muscles of the medium-sized and fine 
bronchi, thus producing an acute pulmonary emphvsema. 
After Bert had shown, in 1870, by experiment that a contrac- 
tion of the medium-sized and finer bronchi could actually be 
produced by irritating the vagus, later Biermer worked out 
his theory so thoroughly, and has defended it so successfully, 
that we are probably justified in accepting it as correct, espe- 
cially as with its help all the characteristic symptoms, the 
sudden onset and the sudden disappearance of the attacks, the 
expiratory dyspnoea, the low position of the diaphragm, etc., 
can well be explained. It is clear that this bronchial spasm 
forms an impediment much more easily overcome by inspira- 
tion than by expiration, and that this difficulty in expiration 
must of necessity not only influence the alveoli, but also the 
smaller bronchi, from which the inspired air can only imper- 
fectly be foixed out ; hence arises dyspnoea and emphysema 
during expiration. On auscultation, sibilant rhonchi are heard 
all over the chest. But all this does not explain the cause of 
the spasm. This may be sought for in an independent affection 
of the bronchial mucous membrane, a view which possibly may 
be supported by the presence in the sputa of asthmatics of the 
so-called " Curschmann's spirals" (spiral threads which must be 
looked upon as casts of the finest bronchioles). Or we may 
assume a reflex origin. Thus Leyden maintained that certain 
pointed octahedral crystals which he discovered in the sputa 
of asthmatics irritated the mucous membrane, and thus pro- 
duced the spasm. Many observations, however, allow us to 
doubt the correctness of this latter view. It has been estab- 
lished, on the other hand, beyond doubt (Voltolini, Hack, Som- 
merbrodt) that certain diseases of the nasal mucous membrane 
(polypous growths, chronic catarrh, etc.) may give rise to asth- 
matic attacks — reflex neurosis ; possibly some part in the pro- 
duction of these is played by the reflex dilatation of the vessels 
in the bronchial mucous membrane, which was by Stork and 
Weber supposed to take place in connection with the bron- 
chial spasm, a theory which was afterward confirmed by Som- 
merbrodt. 

Symptoms. — The characteristic features of the disease are 



H 8 DISEASES OF THE CRANIAL NERVES. 

the paroxysms of distress and dyspnoea, previous to which the 
patient may for days complain of general malaise, be low-spirit- 
ed, and troubled with digestive disturbances, diarrhoea, etc. The 
attacks begin quite suddenly, usually at night, more rarely in 
the day-time ; during them the respiration is changed, so that 
the breathing in inspiration, but more especially in expiration, 
becomes labored and accompanied by a loud wheezing. This 
may last only a few hours or may continue for days, and may 
be repeated at varying intervals. Toward the end of the attack 
moist rales can be heard on ascultation, and there is expectora- 
tion which contains the above-mentioned spirals and crystals. 
Between the attacks the patient enjoys perfect comfort. 

^Etiology. — The aetiology of the disease is but little known. 
No doubt hereditary predisposition does exist, and persons 
with a neuropathic family history fall, cceter is paribus, more easy 
victims to asthma than others. Just of what nature the exciting 
causes of the actual outbreak are we are as yet unable to say. 
We have repeatedly observed that hysterical persons suffer 
from asthmatic conditions, which on examination of the respir- 
atory organs, prove to be of a nervous origin. In these in- 
stances the patients are for days troubled with paroxysmal 
dyspnoea, their expiration is difficult and wheezing, while noth- 
ing abnormal is found on ascultation and percussion. We shall 
later on have more to say about this hysterical asthma. 

That the inhalation of certain kinds of dust may give rise to 
asthma, while not a frequent, is certainly a well-authenticated 
observation. We may especially find this connection when the 
same obnoxious causes have been acting frequently and through 
a rather prolonged period of time, as is the case in those who 
follow certain occupations (millers, bakers, etc.) ; in the same 
way it is well known that repeatedly druggists have been af- 
fected regularly with asthmatic attacks while occupied with the 
pulverization of ipecacuanha root, and that the dust of certain 
kinds of grain — for instance, of oats — causes such disturbances 
in those engaged in thrashing (of. Hirt, Krankheiten der Ar- 
beiter, 1871, Bd. i, p. 12). 

The asthma which develops under the influence of certain 
poisons has to be classed among these cases, and in this con- 
nection the so-called lead asthma (asthma saturninum) is deserv- 
ing of special mention. This is a very peculiar disease, which 
sometimes sets in very acutely only a few minutes after the 
work has been taken up. Though to the highest degree dis- 



DISEASES OF THE VAGUS {PNEUMOGASTRIC NERVE), ng 

tressing to the patient, a fatal outcome in it has never been 
noted (cf. Hirt, op. cit., Bd. iii, p. 40). This trouble is, however, 
even among lead-workers, quite rare, so that we may assume 
that among one hundred affections due to working in lead two 
instances at most of this above-described asthma occur. As to 
the mode of origin, we do not know whether to refer it to the 
action of the poison on the central nervous system, or on the 
peripheral nerve-endings of the vagus. 

Treatment. — We are not acquainted with any specific for 
bronchial asthma ; the much-recommended iodide of potassium 
(2.0-5.0 (xxx to lxxv grs.) a day) often fails, and, as a rule, we do 
not accomplish much with the usual nervines, arsenic, quinine, 
bromide, etc. From the use of electricity we have never seen 
any lasting benefit. Well-conducted hydrotherapeutic meas- 
ures may produce a decided decrease in the frequency and the 
severity of the attacks. For the treatment of the attack itself 
we can foremost recommend pyridin, which was suggested by 
See. It is a product obtained in the dry distillation of organic 
substances, a colorless fluid which easily evaporates in the air. 
For the therapeutic use half a teaspoonful of it has to be poured 
on a shallow dish, and this inhaled three to four times daily in 
a closed room. The smell is horrible, and often disgusting, but 
in many instances the action was found extremely beneficial. 
As soon as the pyridin evaporates the patient becomes easier, 
the feelings of distress are relieved, the heart's action is more 
regular. The effect is not always lasting ; still, I have seen 
cases in which daily regular inhalations used for several weeks 
have not only cut short the individual attacks, but have also 
decreased their frequency. Of course, with this, as with all 
other remedies, we may be disappointed. From the inhalation 
of the fumes of burning saltpetre paper, which has recently 
again been recommended by Kochs, I have only seen transient, 
never any lasting effects. The same holds for the well-known 
stramonium cigarettes, for amyl nitrite, and the vapors of tur- 
pentine. More good may be expected from the administration 
of tinct. lobelia?, which often works like a charm (tinct. lobel., 
5.0 (ni lxxv) ; aquae laurocer., 15.0 ( 3 iv). Sig. : 15 to 20 drops 
every two hours). With the extract of quebracho, which has 
been recommended by Penzoldt, I have no large experience of 
my own. Hyoscyamine, together with small doses of strych- 
nine given several times a day, has been used by Walker (Lan- 
cet, August 20, 1887, p. 368). 



J2Q DISEASES OF THE CRANIAL NERVES. 



LITERATURE. 

Biermer. Ueber Bronchialasthma. Volkmann'sche Sammlung klin. Vortrage, 

1870. 
Mahaux. The Pathogenesis of Asthmatic Attacks. Journ. de Brux., Vol. Ixxiii, 

p. 205, 1881. 
Riegel und Edinger. Deutsche Zeitschr. f. klin. Med., 1882. 
Hack. Ueber eine operative Radicalbehandlung bestimmter Formen von Mi- 

grane, Asthma, Heufieber, sowie zahlreicher vervvandter Erscheinungen, 

1883. 
Schech. Die sogen. Reflexneurosen und ihre Beziehungen zu den Krankheiten 

der Nase und des Rachens. Bayer, arztl. Intelligenzbl., Bd. xxxi, p. 30, 

1884. 
Schaffer. Aus der Praxis: Nasenleiden und Reflexneurosen. Deutsch. med. 

Wochenschr., pp. 23, 24, 1884. 
Sommerbrodt. Mittheilungen von Heilungen patholog. Zustande, welche durch 

Reflexvorgange von der Nase her bemerkt wurden. Berl. klin. Wochen- 
schr., pp. 10, 11, 1884. 
Sommerbrodt. Ueber Nasenreflexneurosen. Ibid., No. 11, 1885. 
See, Germain. Bull, de Therapeut., June 30, 1885, Vol. cviii, p. 529. (Recom- 
mends pyridin.) 
Biermer. Berliner klin. Wochenschr., 41, 1886. 
Kochs. Beitrag zur Kenntniss der Verbrennungsproducte des Salpeterpapieres 

und der Ursachen des Asthma bronchiale. Centralbl. f. klin. Med., Bd. vii, 

p. 40, 1886. 
Grocco, Pietro. Sulla patologia dei nervi cardiaci. Rivist. clin. di Bologna, p. 

12, 1886. 
Dusseaud. De 1'asthme d'origine nasale. These de Paris, 1887. 
Calmettes. Les nevroses reflexes d'origine nasale. Progr. med., No. 28, p. 20, 

1887. 
Fraser. On Dyspnoea, especially on the Dyspnoea of Asthma and Bronchitis, 

and the Effects of the Nitrites upon it. Lancet, July 9, 1887, p. 51. 
See, Germain. Die einfachen Lungenkrankheiten. Translated into German by 

M. Salomon. Berlin, Dammler, 1887. 
Briigelmann. Ueber Asthma. Deutsche Medicinal-Zeitung, 29 et seq., 1888. 

B. Cardiac Affections due to Lesions of the Vagus. 

The superior and inferior cardiac branches are given off from the 
cervical and thoracic portions of the vagus; they join the cardiac 
branches of the sympathetic to form the cardiac plexus (superficial 
and deep). It has not yet been determined of what character these 
fibres are ; there is, however, no doubt but that we have to distin- 
guish inhibitory fibres, the stimulation of which diminishes, and 
accelerator fibres, the stimulation of which increases the number of 
heart beats. The sensory nerves of the heart are also furnished by 
the vagus. 



DISEASES OF THE VAGUS {PNEUMGGASTRIC NERVE). I2 i 

Angina Pectoris. 

Among the neuroses of the heart which probably are caused 
by a disturbance in the vagus, we shall first consider angina 
pectoris (stenocardia, cardiac neuralgia, nervous heart pain), a 
disease of the true nature of which our knowledge is as yet 
quite imperfect, though its symptoms have been recognized 
for more than one hundred years (Heberden, 1772). Its car- 
dinal symptom is a piercing, burning, paroxysmal pain in the 
region of the left nipple, attended with a sensation of impend- 
ing death ; it often radiates into the left arm, and even down 
to the finger tips, and may continue for minutes or hours. It 
usually begins without any premonition and surprises the pa- 
tient by day at his work, or wakes him up at night out of his 
sleep. The severity of the pain differs ; in some cases it is 
moderate, in others it reaches an insupportable degree. Dysp- 
noea is not always present ; the respiration remains sometimes 
regular and quiet, although the patient suffers from a distress- 
ing feeling of anxiety, and his skin is covered with a cold sweat. 
During the intervals, the patient feels perfectly well, unless 
there is a co-existing lesion of the heart muscle or valves. 

The prognosis depends mainly upon the question whether 
we have to deal with a vagus neurosis, or whether some com- 
plication co-exists. If the myocardium, owing to disturbed 
intracardial circulation (caused, for instance, by atheroma of 
the coronary arteries), has undergone pathological changes, 
death may occur during an attack, but this has never to be 
feared if the heart be otherwise sound. It is impossible to 
give an absolutely favorable prognosis with regard to recov- 
ery, because here also we do not possess any remedy which 
is capable of doing away with the attacks entirely. But the 
same suggestions as have been made for the treatment of 
bronchial asthma have been made for angina pectoris, and 
about the same results have been obtained in both. If internal 
treatment can not be dispensed with, digitalis may in the first 
place be tried, then strophanthus, and finally arsenic, which 
latter may with advantage be combined with strychnine. 

For the attacks freshly prepared amyl nitrite, a few drops 
(5 to 10), to be carefully inhaled by the patient, is the most 
useful treatment ; besides this, inhalations of chloroform and 
the hypodermic injections of morphine deserve recommenda- 
tion, as they relieve the patient at once from the intolerable 



122 



DISEASES OF THE CRANIAL NERVES. 



torments of his condition. The severe states of collapse fol- 
lowing these measures, observed by Bamberger, are probably, 
after all, quite exceptional. 

The aetiology of the disease is as obscure as its nature : 
here we must again carefully discriminate between the cases 
where the angina pectoris is merely a symptom of some or- 
ganic heart disease (disease of the coronary arteries, fatty 
heart, valvular disease), and where it appears as an independ- 
ent affection — i. e., where no heart lesion can be demonstrated. 
The latter form is disproportionately less frequent (Gauthier). 
Males and those advanced in age seem especially predisposed 
to the disease (Gauthier) ; yet the author has repeatedly treated 
cases of undoubted angina pectoris in children thirteen to fif- 
teen years of age. Psychical disturbances, such as are found 
in hysterical patients, also the influence of certain poisons — 
e. g., tobacco — deserve some consideration. That angina pec- 
toris is a vagus neurosis can reasonably be accepted, as the 
sensory fibres of the heart are furnished by the vagus, and as 
pain is the most prominent symptom of the trouble. Presuma- 
bly the sympathetic is, however, also concerned, and some are 
even inclined with Lancereaux, who several times found this 
nerve vascularized, to regard the cardiac plexus of the sympa- 
thetic as the chief seat of the disease ; but even were this so, we 
could not exclude some participation of the vagus. A publi- 
cation of Leroux, who found at the autopsy a bronchial gland 
and the right vagus grown together in a case where anginal 
seizures had existed until just before death, appears also to 
speak in favor of an implication of the latter nerve. Fre- 
quently no anatomical lesion was found. 

LITERATURE. 

Lustig. Zur Lehre von den vasomotor. Neurosen (Angina pectoris). Inaug. 
Diss. Breslau, 1875. 

Balfour. Edinb. Med. Journ., March, 1881, Vol. xxvi, p. 769. 

Mackenzie, John N. A Contribution to the Pathology and Treatment of the 
Respiratory Vasomotor Neuroses. New York Med. Journ., February 26, 
1887. 

Huchard. The Weekly Med. Rev., St. Louis, 7, 1887. (Recommends perse- 
verance with iodides — iodide of sodium, gr. xv-xlv daily for a year or a year 
and a half.) 

Le Clerc. L'angine de poitrine hysterique. O. Doin, Paris, 1887. 

Von Basch. Die cardiale Dyspnoe und das cardiale Asthma. Klin. Zeit- und 
Streitfragen, i, 3, 4, 1887. 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). l2 $ 

Nervous Palpitation of the Heart. 

Secondly, we have to speak of the so-called nervous palpi- 
tation of the heart, palpitatio s. hyperkinesis cordis, by which 
term we designate a paroxysmal increase in the frequency and 
strength of the heart's action, which is not only objectively 
noticeable, but also subjectively felt by the patient. Pain is 
absent, and in pure cases at least there is no dyspnoea. Palpi- 
tation appears more frequently as an independent affection than 
angina ; the attacks usually begin suddenly, often at night. If 
the patient be lying on his left side, he is seized with a feeling 
of oppression and anxiety, the pulse is accelerated, and its rate 
may be increased to more than two hundred beats to the min- 
ute ; sometimes the second heart sound is curiously clicking 
(cliquetis metallique) and the first extraordinarily weak, the 
carotids throb, the radial pulse becomes hard and full. Dehio 
(cf. lit.) has examined the pulse curves by means of a Dudgeon 
sphygmograph, and found the pulse waves higher, the decline 
steeper, the first elastic elevation decidedly nearer to the base 
line of the curve, and the dicrotic elevation lower than normal. 
He attributes this condition to an increase in the frequency of 
the beats, and a decrease in the duration of the individual ven- 
tricular contraction. Besides the palpitation, the patient com- 
plains of ringing in the ears, dizziness, and faintness. The 
attacks usually pass off in a few minutes, disappearing as sud- 
denly as they came on, and the patient soon feels perfectly well. 
Their frequency is extremely variable ; they may appear once, 
twice, or more often daily, or only after long intervals of weeks 
or months. 

That here we also have to deal with a neurosis of the vagus 
seems only a rational assumption. The seat varies; it may be 
either central or peripheral, but in most cases we are unable to 
positively say which it is. Sometimes we are justified in as- 
suming that such conditions depend upon a central, bulbar 
nuclear affection, just as we may probably refer a temporary 
diminution of the vascular tonus to a transient paresis of the 
vaso-motor centre in the medulla oblongata (Dehio). 

It is very important in these cases of palpitation to look for 
further co-existing affections, after the removal of which the 
nervous palpitation often disappears suddenly, and never 
recurs. To this class belong chiefly the anasmias of the young, 
cardiogmus juvenilis, habitual constipation, gout, and malaria, 



^4 



DISEASES OF THE CRANIAL NERVES. 



and accordingly we are able to bring about a marked improve- 
ment in the palpitation, which in such cases is only symp- 
tomatic, by improving the condition of the blood, by proper 
regulation of the bowels, by promotion of the excretion of uric 
acid, and by combating malaria by means of quinine, according 
to the indications in each. If such indications for therapeutic 
measures are wanting, we have to fall back upon the narcotics 
and nervines, unreliable as they are in their action. In hyster- 
ical persons certain mechanical manipulations, pressure on the 
abdomen, momentary compression on the neck, and the like, 
may be of service. Application of the ice-bag to the cardiac 
region may occasionally be beneficial ; the psychical treatment 
of the patients, repeated assurances that these attacks are never 
fatal, and that they are quite amenable to treatment, is not to 
be underrated ; in the case of children especially this has been 
found very effectual. 

The aetiology is, unless the palpitation is secondary to an 
underlying disease, quite obscure. Under what conditions 
individuals in other respects quite sound, with a good family 
history, and who present no symptoms of neurasthenia, can 
be attacked by such transient pareses of the vagus we do not 
know. In suspicious cases we should think of masturbation. 

LITERATURE. 

Preisendorfer. Ueber reflectorische Vagusneurose. Deutsches Arch. f. klin. 
Med., xxvii, 3, 4, p. 387, 1880. 

Langer, L. Ueber Vaguslahmung. Wiener med. Wochenschr., xxxi, 30, 31, 
18S1. 

Pick. Prager med. Wochenschr., No. 44, 1884. 

Fothergill. The Gouty Neuroses of the Heart. Edinb. Med. Journ., xxx, p. 
393, November, 1884. 

Semmola, Mar. De l'ataxie paralytique du coeur, d'origine bulbaire. L'Ence- 
phale, vi, 6, p. 413, 1886. 

Dehio. Ueber nervoses Herzklopfen. Petersb med. Wochenschr., August 2d 
and 9th, 1886. 

Mackenzie, Nol. A Contribution to the Pathology and Treatment of the Respira- 
tory Vaso-motor Neuroses. New York Med. Journ., February 26, 1887. 

Tachycardia. 

In rare cases, in people otherwise healthy, but more fre- 
quently in those affected with heart disease, we meet with a 
transient acceleration of the heart's action (tachycardia), which 
usually lasts for several hours, after which the pulse rate again 
becomes normal. These attacks are accompanied by a feeling 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). i 2 $ 

of great anxiety, and are ushered in by vaso-motor disturbances 
— e. g., circumscribed flushings. The number of the pulse 
beats may reach 150 or more. Pressure upon the vagus in the 
neck, a draught of cold water, or similar stimulation of the 
peripheral ends of the vagus often may cut short an attack 
against which we possess no other remedy. Whether in a 
given case irritation of the accelerators or a paroxysmal paral- 
ysis of the vagus is responsible for the attacks has, according 
to Nothnagel (Wiener med. Blatter, i, 2, 3, 1887), to be decided 
in the following way : A great increase in the frequency of the 
pulse, accompanied by a weak heart-beat, and, perchance, 
another disturbance of some nerve path belonging to the vagus, 
speak for paralysis of this nerve ; whereas a strong impulse, 
fullness of the peripheral arteries, with high tension, associated 
with other symptoms of vaso-motor irritation, is in favor of 
stimulation of the accelerators. Traube assumes that some 
cases are due to a temporary anaemia in the medulla oblongata, 
in consequence of which a paresis of the inhibitory nerves en- 
sues. To this class seems to belong the case related by Dehio 
(cf. lit). The mode in which nicotine acts upon the vagus is 
of great interest, and certainly deserves a closer study than has 
been given to it hitherto. 

Chronic nicotine poisoning, as it is found in smokers, and 
only occasionally in tobacco workers, is not always well adapted 
to throw much light on this subject, for, whereas it is well 
known that the nicotine when brought into direct contact with 
the nerves paralyzes them rapidly, it is by no means common 
to find paralysis of the vagus in the course of nicotine intoxica- 
tion. As a rule, it is true that the heart's action is increased, 
yet cases occur in which there is a slowing, so that we are led 
to think of a stimulation of the vagus, such as happens after 
drinking cold water, where the pulse rate may be reduced to 
thirty or twenty beats. Owing to the miserable arrangements 
for ventilation in tobacco factories, we have from time to time 
occasion to study the action of nicotine in those employed in 
them, although the disease is, as has been said, by no means 
frequent. 

Cases which, in consequence of a vagus neurosis, present a 
simultaneous disturbance in the circulatory and respiratory 
apparatus, occur, but are rather uncommon. A case to the 
point has been published by Tuczek (Deutsches Arch. f. klin. 



I2 6 DISEASES OF THE CRANIAL NERVES. 

Med., 1877, xxi, ,1), and two others by Kredel (ibid., 1882, xxx, 
p. 547). For the respiratory apparatus acute emphysema, with 
dyspnoea and symptoms of catarrh, were noted ; they were as- 
sociated with tachycardia (asthma cardiacum, according to 
Kredel), and the existence of a paralysis of the vagus fibres 
regulating the heart, in conjunction with a stimulation of those 
presiding over the lungs, whereby spasm of the muscles of the 
bronchi was produced, was assumed. At the autopsy the 
cause was found to be pressure exerted upon the vagus trunk 
by a rapidly swelling lymph gland. The attacks lasted from 
twelve to thirty-six hours. Some of the patients had organic 
heart disease. 

LITERATURE. 

Langer. Ueber Vaguslahmung. Wiener med. Wochenschr., xxxi, 30, 31, 188 1. 
Probsting. Ueber Tachycardie. Deutsch. Arch. f. klin. Med., Bd. xxxi, Heft 

3 u. 4- 
Dejerine. Neuritis of the Vagi consequent upon the Action of Alcohol. Soc. 

de Biol, de Paris, July 16th and 23d, 1887. 
Dehio. Tachycardie nach der Punction eines Hydrops-Ascites. Petersb. med. 

Wochenschr., 2, May 14th, 1887. 
Farvarges. Ueber die chronische Tabakvergiftung und ihren Einfluss auf das 

Herz und den Magen. Wiener med. Wochenschr., Nos. 11-14, 1887. 
Spengler. Deutsche med. Wochenschr., No. 38, 1887. 
Bristowe. Brain, xxxviii, p. 164, 1887. 

C. The Disturbances of the Digestive Organs due to 
Lesions of the Vagus. 

The vagus forms two gastric plexuses ; the one — the anterior — 
situated on the anterior surface, and the other — the posterior — situ- 
ated on the posterior surface of the smaller curvature of the stomach. 
The first plexus is formed by the left, the second by the right, a 
somewhat stouter nerve. The branches of these plexuses associate 
with fibres from the sympathetic which accompany the ramifications 
of the coronary arteries ; a part of the fibres which appertain to the 
right (posterior) vagus go on to the cceltac plexus, and can in a 
careful dissection be traced to the spleen, the liver, the kidneys, and 
small intestine. 

The muscles of the oesophagus and stomach are also innervated 
by the vagus; its sensory fibres conduct the impulses concerned in 
the reflex actions of deglutition, sobbing, and vomiting. 

One of the digestive disturbances attributable to an affec- 
tion of the vagus, the so-called gastroxynsis, has been men- 
tioned in the consideration of migraine; another one, which 



DISEASES OF THE VAGUS (PNEUMOCASTRIC NERVE). i2 y 

occurs paroxysmally — namely, the gastric crisis (Charcot), 
which depends presumably upon an affection of the nucleus of 
the vagus — will be discussed in the description of tabes. It 
remains, therefore, to speak of three groups of symptoms, two 
of which are quite frequently met with, constituting in them- 
selves separate diseases — namely, cardialgia and nervous dys- 
pepsia — while the third one, the so-called cesophagismus, is 
more frequently observed as a symptom of other neuroses, 
especially hysteria. 

Cardialgia. 

Cardialgia (gastralgia, gastrodynia) is a disease of the sen- 
sory nerves which occurs mostly in paroxysms. Romberg, 
distinguishing two forms, assumed the one to be due to a 
hyperesthesia of the vagus branches going to the stomach 
(" gastrodynia neuralgica"), the other to a hypersesthesia of the 
solar plexus (neuralgia cceliaca). There have been, however, 
cases coming under notice which can not be classed under 
either of these heads, and even more which do not permit of 
a decision as to which of the two forms we are dealing with. 

The characteristic symptoms of gastrodynia are violent 
paroxysmal constricting pains, starting in the region of the 
stomach and radiating to the back ; the face becomes livid, 
hands and feet cold, the pulse smaller and intermittent, and a 
feeling of unutterable anguish and distress takes possession of 
the patient. If in the presence of these symptoms careful ex- 
amination has excluded the existence of any organic stomach 
lesion — e. g., acute or chronic catarrh, gastric ulcer or tumor 
— if there is no evidence of gall stones, and the patient has pre- 
viously at times been subject to neuralgia in other parts of his 
body, we make our diagnosis with some amount of certainty. 
But in all cases this can only be done after careful and repeated 
examination before and after meals ; not uncommonly we find 
that pain, which is present while the stomach is empty, is re- 
lieved by the ingestion of food, and the patient states that 
uniform firm pressure on the epigastrium has often a beneficial 
alleviating effect, both conditions not generally observed in 
organic diseases of the stomach. 

In the treatment of these cases we must first of all en- 
deavor to remove any primary cause, and in this connection 
mental and physical overstrain, excesses in venery, masturba- 
tion, uterine affections, must be thought of. Besides the ex- 



I2 g DISEASES OF THE CRANIAL NERVES. 

ternal application of blisters to the epigastrium, arsenic given 
for several weeks is to be recommended. During the attack 
morphine can often not be dispensed with. The diet has to 
be carefully regulated, but not restricted ; on the contrar}^, it 
is advisable for the patient to take four or five times daily 
substantial but easily digestible food. 

LITERATURE. 

Sawyer, J. Clinical Lecture on the Treatment of Gastralgia. Lancet, August 
13, 1887. 

Nervous Dyspepsia. 

The disease known as nervous dyspepsia is an extremely 
common neurosis of the vagus, especially in females. It is 
characterized by a loss of appetite, painful sensations in the 
region of the stomach, frequent vomiting, and still more fre- 
quent belching ; besides these the patients generally suffer 
from other nervous symptoms — dull headache, vertigo, palpita- 
tion — they are easily tired, complain of a lump in their throat 
(globus hystericus), at times have a voracious appetite, and 
obstinate constipation is seldom absent. In rare cases periodi- 
cal spells of vomiting have been noted (twenty to thirty in 
the twenty-four hours), accompanied by acute circumscribed 
swellings of the skin (angio-neurotic oedema, Striibing, 
Quincke). Although the patients feel very poorly, their 
state of nutrition remains, nevertheless, for a long time re- 
markably good ; only in a few cases do we observe a rapidly 
increasing and marked anaemia. It is still doubtful whether 
the condition is essentially a disease of the peripheral nerves 
of the stomach or a general neurosis (neurasthenia dyspeptica, 
Ewald). We would refer the reader to a most interesting and 
comprehensive article which has been written on this subject 
by Leube (Berl. klin. Wochenschr., No. 21, 1884). 

In making our diagnosis we are brought face to face with 
no inconsiderable difficulties. The claim of Leube that we are, 
in the presence of the above-described symptoms, justified in 
thinking of nervous dyspepsia if a stomach-washing six to 
seven hours after the meal shows the stomach to be empty, 
has been opposed by Ewald and others. These have shown 
that, on the one hand, the stomach may be empty seven hours 
after a meal in cases of ulcer, and, on the other hand, may 
contain remains of food in nervous dyspepsia after the same 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). \ 2 g 

time. To be sure, an increase of hydrochloric acid (hyper- 
acidity) is a common condition in gastric ulcer. The results 
of stomach-washing are, however, certainly not always pathog- 
nomonic, but we must rather for the purpose of diagnosis take 
into account the course of the disease and the general condi- 
tion of the patient. But in spite of the greatest care experi- 
enced men not seldom in these cases are led into error. Un- 
der certain circumstances the hyperemesis nervosa, a motor 
neurosis of the stomach occurring in pregnant women, espe- 
cially in the first months of pregnancy, may closely simulate 
this disease. 

In the treatment our attention has chiefly to be directed to 
the proper nutrition of the patient. Of medicines, arsenic, 
quinine, chloral (i.o (grs. xv) several times a day), should be 
resorted to. Saline purgatives, Carlsbad water, as well as the 
use of electricity, are of no avail. A stay in the mountains, 
hydrotherapy, sea-baths, all should be tried in succession, and 
last, but not least, the possibilities of psychical treatment must 
not be forgotten. 

LITERATURE. 

Cherchewsky. Contributions a la pathologie des nevroses intestinales. Revue 

de med., 3, 1884. 
Schiile. Arch. f. Psych, u. Nervenkrankheiten, xv, 3, 828, 1884. (Nervous 

Dyspepsia, with a Reflex Vagus Neurosis as a Complication. — Respiratory 

Difficulty.) 
Allbutt. Visceral Neuroses. Lancet, i, 11, 12, 14, 1884. 
Hiring. Die nervose Dyspepsie und ihre Folgekrankheiten. v. Volkmann's 

Sammlung klin. Vortrage, No. 283. 
Neustab. Neuroses of the Stomach. Russ. med., 26-28, 1887. 

(EsopJiag ismus. 
Spasmodic dysphagia, known as cesophagismus (spasm of 
the gullet), is an affection which sometimes follows dyspeptic 
symptoms and protracted vomiting, sometimes irritation of the 
fauces by hot food, irritating substances (mushrooms, red pep- 
per, etc.). Sometimes the spasm is seen to occur reflexly in 
consequence of uterine diseases, and quite frequently in hys- 
teria. As an independent affection it is rarely ever observed. 
In all cases it is characterized by the fact that the patient from 
time to time (periodically) experiences great difficulty, or is 
even unable, to swallow his food, that when it reaches a cer- 
tain point it is regurgitated, and that the sound which is intro- 
9 



130 



DISEASES OF THE CRANIAL NERVES. 



duced for the purpose of examination is stopped at the same 
place ; if this point is situated in the upper portion of the 
oesophagus, usually violent pain is experienced on the inges- 
tion, more especially of cold food, a circumstance which makes 
the patient object to taking his nourishment, and consequently 
leads to emaciation, although the loss of flesh is here much less 
considerable than in stenosis of the oesophagus caused by new 
growths, because in the former case the patient is able at times 
to swallow his food without any difficulty. 

Predisposed to cesophagismus are nervous, easily excitable, 
hysterical persons in whom the affection often suddenly makes 
its appearance after some emotion without the previous exist- 
ence of any symptoms referable to the oesophagus. It has 
often followed the suppression of the menses, or has appeared 
during pregnancy and lactation. Sometimes no other setio- 
logical factor could be discovered than injuries to the gullet 
years previous to the spasm — burns, injury by sulphuric acid, 
etc. No definite statement is warranted as to the duration and 
the course of the disease, as both vary greatly, but this much 
may be said with certainty, that in pure cases the prognosis is 
always good, that complete recovery is almost always effected 
by the repeated use of the sound and by the application of the 
faradic brush. 

LITERATURE. 

Chamaillac. Journ. de med. et de chir. prat., p. 311, 1846. 

Matthieu. Gaz. med. de Lyon, p. 102, 1852. 

Gendron. Arch, gener., 5me ser., t. xi, p. 293, 1858. 

Vigla. Gaz. des hop., Septembre 25, 1869. 

Axenfeld. L'Union, 73, 1872. 

Hulke. Transact, of the Clin. Society, vol. vi, 1873. 

Roux. These de Paris, No. 105, 1873. 

Smith. Dubl. Quart. Journ., March, 1864. 

Peter. Gaz. des hopit., 85, 1875. 

Mackenzie, Morell. Med. Times and Gaz., October 21, 1876. 

Eloy. Contribution to the Knowledge of CEsophagismus. Gaz. hebd., 2me 

serie, t. xvii, 46, 47, 50, 1880. 
Strubing. Ueber acutes angioneurotisches CEdem. Zeitschr. fur klin. Med , Bd. 

ix, 5, 1885. 
Meltzer. Ein Fall von Dysphagie nebst Bemerkungen. Berl. klin. Wochen- 

schr., 8, 1888. (Symptoms of oesophagus-stenosis lasting for nineteen 

years.) 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). y^I 

D. Graves' Disease— Basedow's Disease {Glotzaugenkrank- 
heit, Cachexie exophthalmique) — EXOPHTHALMIC Goitre — 
Tachycardia strumosa exophthalmica. 

Symptoms. — The three symptoms which are regarded as 
characteristic of Graves' disease are (i) an excited, accelerated 
action of the heart, with visible pulsation in the arteries of the 
neck ; (2) enlargement of the thyroid gland ; (3) exophthalmos. 
As a rule the heart symptoms are the first to appear. The 
increase in the frequency of the pulse is variable. We may 
count from a hundred to a hundred and fifty beats a minute, 
and not infrequently the intensity of the heart beat is more 
forcible than normal, a circumstance which adds much to the 
discomfort of the patient. Auscultation does not always re- 
veal abnormalities. Occasionally a systolic souffle is audible, 
but this is often absent. Enlargement of the heart also has 
been observed. The extraordinarily strong pulsation in the 
carotids, which is very conspicuous and easily felt, is in re- 
markable contrast to the smallness of the pulse wave in the 
radial artery (Parry). 

The swelling of the thyroid is rarely very great. It is usu- 
ally symmetrical. In the gland itself pulsation can be easily 
seen, and on palpation a distinct thrill is communicated to the 
hand. I may say that I have repeatedly seen cases in which 
the volume of the gland changed from time to time, and that 
this change became perceptible in a comparatively short time, 
sometimes even in a few hours. 

The exophthalmos, which is probably always bilateral, also 
differs in degree in different cases. In the majority, however, 
it is so marked that the protruding eyeballs can not be com- 
pletely covered by the lids during sleep. This gives to the 
patient an appearance which to the layman is both peculiar 
and repulsive, and is still more aggravated if the upper eyelid 
does not follow the downward motion of the ball, and thus 
allows a zone of the sclerotic, 1 to 2 mm. in width, to become 
visible above the cornea. This defective co-operation of lid 
and ball (Graefe's symptom), which happily does not occur 
very often, makes the patient almost an object of horror to 
those who surround him. The almost complete absence of the 
involuntary winking of the lid (Stellwag's symptom) is quite 
conspicuous, especially since the voluntary movements can be 
made as well as before. We can then easily understand that 



132 



DISEASES OF THE CRANIAL NERVES. 



our patients, particularly when they are ladies of the better 
classes, avoid as far as possible the contact with friends and 
acquaintances, as well as with strangers. 

Ophthalmoscopically only one characteristic sign has been 
noted — namely, the spontaneous pulsation of the retinal vessels, 
discovered by O. Becker. This is not confined to the disk, 
but can be observed in the retina as well. With this exception 
there are no changes in the fundus and eye-sight, accommoda- 
tion, and pupils are entirely normal. Only on the cornea we 
occasionally find a decrease in sensibility, probably due to the 
want of moisture on the ball, the normal quantity of the lachry- 
mal fluid not being sufficient on account of the undue evapora- 
tion which takes place, because the two lids are far apart, and 
winking only rarely occurs. 

Insufficiency of convergence, a symptom first described by 
Mobius, is sometimes observed. If the patient be asked to 
look at a near point, one eye will soon be found to deviate out- 
ward. 

Among the subjective symptoms, in addition to the annoy- 
ing palpitation already mentioned, a tendency to free perspira- 
tion may be noted. Even slight exertion produces a feeling of 
heat, more especially in the head and neck, so that the patient 
preferably remains in cool, shady places, and sleeps with as 
little covering as possible, etc. An actual elevation of temper- 
ature is, however, not always objectively demonstrable. This 
tendency also accounts for the blushing evoked by the least 
bodily exertion or mental emotion. Both symptoms I have 
not infrequently seen to occur unilaterally. Trousseau has 
mentioned the fact that the most gentle stimulation of the skin 
of the face and neck produces a deep-red mark, designated by 
him as tdche cerebrate, a phenomenon, however, which can ap- 
parently not always be evoked. All these symptoms are at- 
tributable to asthenia of the vaso-motor nerves, as is also the 
decrease in the resistance which the skin offers to the elec- 
trical current, first observed by Charcot, the saturation of the 
skin with fluid resulting from the dilatation of its capillaries 
rendering it a better conductor than it would naturally be in 
the dry state. In a healthy individual using an electro-motive 
force of from ten to fifteen volts the resistance amounts to from 
four to five thousand, ohms, while in the course of this disease 
it only measures from three to six hundred ohms, and only in- 
creases when the patient improves. 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). 



133 



Various nervous disturbances often accompany Graves' dis- 
ease, among which the copious vomiting of a watery bile must 
be considered the most important. It may be of such persist- 
ency as to seriously reduce the strength of the patient. Ver- 
tigo, buzzing in the ears, sleeplessness, occasional transient 
dyspnoea, have also been observed. Falling out of the hair of 
the head and eyebrows is not rare, and I have seen a case of a 
peasant woman, thirty-eight years old, who, toward the end of 
the disease, when she was extremely emaciated owing to the 
persistent diarrhoea and vomiting, had become completely bald. 

Complications with chorea, epilepsy, and diabetes mellitus 
are said to occur. Oppenheim has described a case in which 
it accompanied Addison's disease (Neurologisches Centralblatt, 
i, p. 29, 1888). 

Course. — We should keep in mind that remissions may 
occur during the course of the disease ; nay, that it often may 
remain stationary for months or years before further deteriora- 
tion takes place which leads to death. For our prognosis a 
knowledge of the fact that such remissions can occur is of 
great importance. Cases which pursue a rapid course from 
the very beginning are exceptional. 

The onset, of the disease may be either brusque or quite 
gradual. In the first case twelve to fourteen hours are suffi- 
cient time for the development of the three cardinal symptoms ; 
in the latter these appear gradually — first the palpitation, then the 
swelling of the neck, and finally the protrusion of the eyeballs. 

Of great interest, because relatively frequently met with, 
are the cases in which the disease does not reach its full devel- 
opment; only certain symptoms are well marked, while others 
may be hardly perceptible or even absent. Trousseau calls 
these instances "formes frustes" {fruste — abortive), and attrib- 
utes much importance to them. P. Marie has subjected them 
to a careful study in his excellent monograph (cf. lit.), and has 
shown that the goitre as well as the exophthalmos may be 
wanting, in which case we shall only find the tachycardia, very 
often accompanied by a symptom to which he has given special 
attention — namely, the tremor. This tremor shows a great 
regularity of rhythm, and consists of about eight or nine 
oscillations in a second. Ernst Cramer, in his observations 
made in my wards, was generally able to confirm Marie's re- 
sults. (Ueber das Wesen des Zitterns. Inaugural Disserta- 
tion. Breslau, 1886.) 



! 3 4 DISEASES OF THE CRANIAL NERVES. 

Prognosis. — The prognosis seems to be less favorable in the 
male sex and in advanced age than in female patients, the latter 
always having a better chance, especially if pregnancy inter- 
rupts the disease (Charcot). 

Etiology. — iEtiologically the affection is obscure. Pelvic 
diseases, cold, emotions, hereditary tendencies, have been 
thought of in this as in other neuroses, but their causative 
action does not seem even probable. 

Pathological Anatomy. — What has been found on the au- 
topsy table does not give us any key to an understanding of 
the disease, for all that has been observed in the cervical sym- 
pathetic is very inconstant, and although an enlargement and 
thickening of its ganglia has several times been met with, we 
are not justified in drawing any conclusions from such altera- 
tions, especially as there are cases published in which the ex- 
amination of the sympathetic gave entirely negative results. 
The changes in the heart and thyroid were equally unsatisfac- 
tory. Only one thing more I should like to mention, namely, 
that often immediately after death the exophthalmos is mark- 
edly smaller than during life, or at times entirely disappears. 

Pathogenesis. — To explain, then, the pathogenesis of the 
disease is difficult. Certainly, however, the explanation of Ko- 
bens, afterward defended by Trousseau, Fletscher, Reith, Eu- 
lenburg, Guttmann, and others, that the disease was essentially 
one of the sympathetic, is, to say the least, doubtful. Without 
taking into consideration the fact that we should in this case be 
obliged to assume a constant state of irritation of certain groups 
of fibres in the sympathetic, the goitre and exophthalmos can 
hardly be explained by lesions in this nerve. For these reasons 
Sattler proposed to assume a circumscribed lesion in the region 
of the vagus centre, by which the inhibitory action on the heart 
is diminished or suspended. He does not consider that the ab- 
sence of other vagus symptoms can be held to disprove this, as 
this inhibitory action actually can be suspended and the other 
functions of the nerve remain intact. Filehne, who cut the 
restiform body in its anterior quarter, and thus produced symp- 
toms of Graves' disease, is also inclined to make a lesion of the 
pneumogastric responsible for at least some of the symptoms. 
Goitre and exophthalmos are, according to him, due to a vaso- 
motor paralysis. Broadly the whole disease is, in his opinion, 
of a paralytic nature. 

All attempts to fix the anatomical seat of the disease have 



DISEASES OF THE VAGUS (PNEUMOGASTRIC NERVE). ^5 

this disadvantage in common, that they only explain a part of 
the symptoms. It seems therefore, in view of our defective 
knowledge, more reasonable to collect and analyze more obser- 
vations before adding a new hypothesis to those already ex- 
isting. 

Sattler attributes Graefe's symptom to a lesion of a co-ordi- 
native centre which governs the co-operation of the levator 
and orbicularis palpebrarum on the one hand, and of the mus- 
cles which rotate the eye round its horizontal axis on the other. 
Stellwag's symptom he explains by a lesion in the centre which 
communicates reflexes, starting from the retina and the sen- 
sory fibres of the conjunctiva and cornea to the motor apparatus 
of the lids. 

Treatment. — The treatment in most instances is not at- 
tended with much success. In so many cases, which received 
no treatment whatever, improvement has been noticed, that 
our therapeutic measures, although at times giving apparently 
good results, are not too much to be relied upon. As a rule, 
internal medicines are the least efficient. Iron and quinine are 
those generally in use, but little is accomplished by them. The 
same must be said of the iodide and the bromide of potassium. 
Opiates and ergot have also been tried, but without result. 
More may be expected from hydrotherapy, whether it be in 
the form of Priesnitz's cold packs or of cold douches, which 
latter should be used for a considerable time. Patients of the 
better classes should remain several months of the year in 
properly conducted hydrotherapeutic establishments, as most 
of them will generally feel more comfortable there than at 
home. The best success, after all, is obtained, according to my 
own observations, from systematic galvanic treatment. The 
cathode is applied to the angle of the lower jaw, while the 
anode is held at the lower cervical vertebrae (on the opposite 
side). The current should be weak, and only applied for a 
short time, from a minute to a minute and a half. Not infre- 
quently after the tenth or fifteenth seance, not generally until 
after the twentieth or thirty-fifth, we are able to observe a 
steadily progressing improvement which may last for years 
(Erb, Benedict, Guttmann, Mor. Meyer, and others). Whether 
this is due to the action on the sympathetic or on the vagus 
can not be decided, as both nerves are influenced by the elec- 
tricity. 

That some cases of Graves' disease have a peripheral origin 



jo6 DISEASES OF THE CRANIAL NERVES. 

is shown by the communications of Hack (cf. lit.), who repeat- 
edly succeeded in removing some symptoms of the disease — 
for instance, the exophthalmos — by destruction of the swollen 
erectile tissue of the nose by the galvanic cautery. On the 
operated side the eye at once went back to its normal size, a 
fact which should impress us with the necessity of always 
making a rhinoscopic examination. 



LITERATURE. 

Basedow, v. Exophthalmus durch Hypertrophic des Zellgewebes in der Augen- 
hohle. Casper's Wochenschr. f. d. ges. Heilkunde, No. 13, p. 197, and No. 
14, p. 220, 1840. 

Koben. De exophthalmo ac struma cum cordis affectione. Diss, inaug. Bero- 
lini, 1855. 

Charcot. Sur la maladie de Basedow (cachexie exophth.). Gaz. hebdom., No. 

14. 1859- 

Trousseau. Du goitre exophth. Union med., Nos. 142, 143, 145, 147. Gaz. 
hebdom., pp. 219, 267, Gaz. des hop., Nos. 139, 142, i860. 

Oppolzer. Ueber Basedow'sche Krankh. Wien. med. Wochenschr., Nos. 48, 
49, 1866. 

Chvostek. Weitere Beitrage zur Pathologie und Elektrotherapie der Basedow'- 
schen Krankheit. Wien. med. Presse, Nos. 23, 27, 32, 39, 41-46, 1872. 

Meyer, M. Ueber Galvanisation des Sympathicus bei der Basedow'schen Krank- 
heit. Vortrag, gehalten in der Berl. med. Ges. v. 17. Juli. Berl. klin. Woch- 
enschr., Nos. 19, 20, 1872. 

Eulenburg and Guttmann. Die Pathologie des Sympathicus. Berlin, p. 32 et 
seq., 1873. 

Eulenburg. Vasomotorisch-trophische Neurosen. Die Basedow'sche Krankh., 
p. 73. 1875- 

See, Germain. Symptomes de la maladie de Basedow. France med., No. 87 
et seq., 1878. 

Filehne. Zur Pathologie der Basedow'schen Krankheit. Sitzungsbericht der 
physik.-med. Societat zu Erlangen, July 14th, p. 177, 1879. 

Guttmann, P. Basedow'sche Krankheit. Eulenburg's Real-Encyclop. der ges. 
Heilkunde, Bd. ii, p. 15, 1880. 

Sattler in Grafe-Samisch' Handbuch der Augenheilkunde, Bd. vi. Leipzig, En- 
gelmann, 1880. 

Marie, P. Contribution a 1'etude et au diagnostic des formes frustes de la mala- 
die de Basedow. Paris, aux Bureaux du Progr. med., 1886. 

Jendrassik. Arch. f. Psych u. Nervenkrankheit, xvii, p. 301, 1886. 

Mobius. Centralblatt fur Nervenheilkunde, 12, 1886. 

Hack. Arch. f. Psych, u. Nervenkrankheiten, xviii, p. 274, 1887. (Cure of 
Graves's disease by galvano-caustic treatment of abnormal swelling in the 
nose.) 

Durdufi. Zur Pathogenese des M. Basedowii. Deutsche med. Wochenschr., 
No. 2i, 1887. 



DISEASES OF THE VAGUS {PNEUMOGASTRIC NERVE). i$j 

Sainte-Marie, M. Contribution a l'etude de la maladie de Basedow. These de 

Paris, 1887. 
Vigouroux. Sur le traitement et sur quelques particularites cliniques de la mala- 
die de Basedow. Progr. med., No. 43, 1887. 
Wolfenden. A New Point in the Diagnosis of Graves' Disease. Practitioner, 

234, 1887. (Treats of the diminution of the resistance to conduction of 

electricity.) 



CHAPTER IX. 

THE DISEASES OF THE ACCESSORY NERVE. 

The accessorius consists of two parts, both of which have a sepa- 
rate origin and exit. The upper one belongs entirely to the vagus, 
emerges with it, and is hence called accessorius vagi. The lower one 
begins at the level of the first cervical nerve (cf. Fig. 27), and can be 
traced as far down as the level of the sixth, sometimes even of the 




r_p.cn: 



Fig. 27.— Cross-section through the Cervical Cord. r.p.C.II, posterior root of 
the second cervical nerve. XI, fibres of accessorius. C. a., anterior horn. C.p., poste- 
rior horn. C. L, lateral horn. H l , Goll's column. H 2 , Burdach's column. S, lateral 
column. V, anterior column, g, substantia gelatinosa of posterior horn. 



seventh cervical nerve roots ; this is the spinal portion, the accesso- 
rius spinalis. After having passed upward to the foramen magnum, 
close to the cord, it unites inside the skull with the portion belong- 
ing to the vagus to form for a while a common trunk, the accessorius 
communis, which, soon after leaving the skull through the jugular 
foramen, again divides into two branches, the accessorius vagi then 
becoming the inner, the accessorius spinalis the outer branch. 



THE DISEASES OF THE ACCESSORY NERVE. 



139 



The nucleus of the former portion has been described in the two 
previous chapters; that of the spinal portion is in the region of the 
anterior horn of the cervical cord. Since the latter is provided with 
motor ganglionic cells, the purely motor nature of the spinal portion 
is evident (Schwalbe). According to Dees (Allgem. Zeitschr. f. 
Psychiatrie von Laehr, Bd. 43, Heft 45, 1887), the nucleus of the 
accessorius is divided into three portions, the upper being situated in 
the centre of the anterior horn, just above the first cervical nerve; 
the middle at the lateral border of the anterior horn from the second 
to the fourth cervical nerve ; and the lowest at the base of the lateral 
horn from the fourth to the sixth cervical nerve. The large multi- 
polar (motor) ganglionic cells which form the nucleus are arranged 
like a rosary. 

We may have central as well as peripheral diseases of the 
accessorius, and, as is the case in other motor cranial nerves, 
the diseases may be of a paralytic or of an irritative nature 
(hyperkinesis, spasm — akinesis, paralysis). 

Accessorius Spasm, Spasmodic Wryneck, Spasmodic 
Torticollis {Tic Rotatoire, Nickkrampf). 

Since the accessorius supplies the sterno-cleido-mastoid and 
the trapezius (with its posterior larger portion), it is these two 
muscles which present disturbances in affections of the nerve. 
Either of them may be affected by itself, by a clonic or a tonic 
form of spasm ; hence there exist quite a variety of clinical 
pictures, especially as the disease may also be unilateral or bi- 
lateral. The sterno-cleido-mastoid is about as often the seat 
of a clonic spasm as the trapezius, whereas the tonic form is 
very rarely seen in the latter muscle. 

By the rhythmical contractions of one sterno-cleido-mastoid 
the head is moved to one side in a very characteristic manner ; 
the chin is turned toward the opposite (well) side and is ele- 
vated, while the ear is approached to the clavicle. Contracture 
of this muscle (the tonic spasm) fixes the head in this position 
— caput obstipum spasticum. If both sterno-cleido-mastoids 
are affected, the head is drawn alternately first to the one, then 
to the other side (clonic form), or it is pulled strongly forward 
and bent toward the chest (tonic form of the spasm). 

Contractions of the trapezius draw the head backward and 
toward the diseased side, elevate the shoulder, and approach 
the scapula to the vertebral column. A tonic spasm in the 
same locality entails fixation of the head in this position. 



14-0 



DISEASES OF THE CRANIAL NERVES. 



A simultaneous spasm of the sterno-cleido-mastoid and the 
trapezius of the same side, in which the facial muscles also 
sometimes take part, is known to occur more frequently than 
an affection of both trapezii or of both sterno-cleido-mastoids 
alone. The directions of the movements and the positions 
which result from such spasms can be made out from what has 
been just said. 

The occurrence of such affections is either in paroxysms or 
else we have permanent contractions, only ceasing or abating 
during sleep. Recovery is exceptional. All therapeutic meas- 
ures, not excluding the electrical and chirurgo-orthopsedic 
treatment, are usually unsuccessful. The thermo-cautery may 
be tried. Any internal medication would have to be con- 
ducted according to the principles described in the treatment 
of facial spasm. 

The causes of the disease differ widely. Cerebral tumors, 
meningitis, foci of softening, as well as caries of the cervical 
vertebras, new growths in the medulla oblongata, may give rise 
to central, while external influences, cold, etc., may give rise to 
peripheral affections of the nerve. There are, moreover, well- 
authenticated cases on record of reflex spasm in the distri- 
bution of the accessorius arising from irritation by worms, 
uterine trouble, fright, and other emotions. As a rule, no 
^etiological factor can be detected. An epileptic who came 
under my observation, a single woman, twenty-seven years of 
age, presented at times a spasmodic torticollis, the contractions 
being extremely violent, sometimes lasting for weeks, and again 
being almost entirely absent for the same length of time. 

Accessorius Paralysis. 

This very rare disease may take in one or both of the 
above-named muscles. Unilateral paralysis of the sterno-cleido- 
mastoid produces a wry position of the head, in which the chin 
is somewhat elevated and directed toward the diseased side. 
Turning of the head is difficult but not impossible, as other 
muscles are brought into play. Bilateral paralysis of the muscle 
causes the head to be held straight, and is characterized by the 
absence of the prominence which the normal muscle produces. 

Unilateral paralysis of the trapezius allows the scapula to 
sink downward, causing the distance between its internal mar- 
gin and the vertebral column to become greater. As a con- 
sequence, the arm falls forward, the clavicle becomes more 



THE DISEASES OF THE ACCESSORY NERVE. 



141 



prominent, the supraclavicular fossa more marked, and the 
posterior upper angle of the scapula can be distinctly felt. 
Voluntary elevation of the shoulder and the motion of the 
scapula toward the spinal column is interfered with, and be- 
comes only possible with the aid of the levator anguli scapula? 
and the rhomboidei. The arm can not well be raised above 
the horizontal position in spite of the serratus which acts nor- 
mally, because the action of the upper third of the trapezius is 
lost. The paralysis of both trapezii allows both shoulders to 
sink outward and forward, so that the back appears more 
curved ; the ability to support the head in the upright posture 
is sometimes interfered with. Simultaneous paralysis of the 
sterno-cleido-mastoids and the trapezii gives a combination of 
both clinical pictures. If, in addition, the inner (smaller) por- 
tion of the nerve takes part, the resulting paralysis of the 
laryngeal muscles, the velum palati, and the pharyngeal mus- 
cles manifests itself by hoarseness, the nasal tone of the voice, 
and difficulty in swallowing. The increase in the frequency of 
the pulse, which has in such cases been observed by Seelig- 
miiller, must be attributed to the simultaneous affection of the 
cardiac branches of the vagus. Prognosis and treatment are 
the same as in the spasmodic affections, and little more can be 
said about the astiology. Yet we should add here that these 
forms of paralysis have been known to occur in consequence of 
certain occupations (water-carriers, whose occupation obliges 
them to carry buckets suspended from their shoulders, and 
who are exposed to wettings, are apt to suffer- — Seeligmiiller), 
and in the course of tabes it has been seen as a bulbar affection. 
We may also imagine an injury to the nuclei of the nerve 
during difficult labor, and in symptoms of paralysis in the mus- 
cles of the neck in new-born children, who for the first few 
years of life are unable to hold the head straight, such a possi- 
bility ought not to be forgotten (Gowers). 

LITERATURE. 

Seeligmiiller. Arch. f. Psych., iii, 2, p. 433, 1872. 

Kropff. Beobacht. iiber Krampfe im Bereiche des Accessorius und der oberen 

Cervicalnerven. Diss, inaug., Gottingen, 1875. 
Remak. Doppelseitige Lahmung des Accessorius Willisii. Deutsche med. 

Wochenschr., 27, 1885. 
Duchenne-Wernicke. Physiologie der Bewegungen, p. 588 et seq. Cassel u. 

Berlin, 1885. 
Martius. Berliner klin. Wochenschr., No. 8, 1887. 



CHAPTER X. 

DISEASES OF THE HYPOGLOSSAL NERVE. 

The ten to fifteen bundles of fibres of which the hypoglossal 
nerve consists, as it emerges from the medulla oblongata in the 
groove between the anterior pyramid and the olivary body, unite to 
form two larger bundles, which leave the dural space separately, and, 
aftei their entrance into the hypoglossal canal, the anterior condyloid 
foramen, become a single stem, which leaves the cranial cavity by 
this canal. Outside the base of the skull it passes along to the 
mesial side of the vagus, at first obliquely downward and forward, 
then obliquely upward, runs on the outer surface of the hyoglossus 
muscle, and soon reaches the region where the genioglossus muscle 
radiates into the tongue. There are various communications be- 
tween the hypoglossus, the vagus, the anterior branches of the upper 
cervical nerves, and the lingual branch of the trigeminus. The su- 
perficial origin of the hypoglossal nerve and of the other cranial 
nerves and their points of exit from the brain-substance and the 
base of the skull are represented in Figs. 28 and 29. 

The cortical area of the hypoglossal nerve is found, according to 
Exner, in the lower portion of the anterior central convolution and 
the adjoining portion of the inferior frontal convolution, as shown in 
Fig. 30. Its nucleus is situated in the floor of the fourth ventricle 
(Fig. 37), where its very large ganglionic cells, which measure up to 
60 n in diameter, closely resemble the large multipolar ganglionic 
cells of the anterior horn in the cord. 

The root fibres of the hypoglossus (Fig. 31, 12) certainly arise in 
part from the nucleus of the same side. To what extent the nucleus 
of the opposite side, as well as the group of ganglionic cells situated 
in its neighborhood and the above-mentioned nucleus ambiguus (Fig. 
31, Xa), can be considered sources of origin for them, and, moreover, 
whether direct fibres of the hypoglossus have their origin in the cere- 
brum, is still undecided. 

While in certain of the cranial nerves — for instance, in the 
facial — peripheral affections occur at least as frequently as cen- 



DISEASES OF THE HYPOGLOSSAL NERVE. ^3 

tral, in the case of the hypoglossal this is not true. Often as 
its nuclei take part in the most diverse diseases, especially of 
the cord and medulla oblongata, it is rare that a peripheral 
affection comes under observation. That, in a given case, the 




ca 



Fig. 28. — Superficial Origin of the Cranial Nerves. I-XII, the twelve cranial 
nerves. CI, anterior root of the first cervical nerve, ca, anterior column of the spinal 
cord, cl, lateral column, pa, anterior pyramids, o, olivary body. P. V., pons Varolii. 
i, internal geniculate body, e, lateral geniculate body, tc, tuber ciner. //, pituitary 
body. P, cerebral peduncle. Sy, region of the fissure of Sylvius, a, corpora albicantia. 
C, island of Reil. Th, optic thalamus. 

disturbance is peripheral and not central, more especially not 
bulbar, we may conclude from the absence of other symptoms 
of bulbar disease, and from the possible presence of complete 
reaction of degeneration, as Erb (cf. lit.) has done in his recent- 
ly described case. The sj^mptoms otherwise are the same as in 
the central disease. 



144 



DISEASES OF THE CRANIAL NERVES. 



Central paralysis of the hypoglossus may be, in the first 
place, of cortical origin. According to Exner, as has been 
stated, the cortical area for the tongue is situated at about a 
point where the middle and inferior frontal convolutions join 




viii, acust. 



ix, gl. ph. 



xii, hypg. 



Fig. 29. — Base of the Skull with the Emerging Cranial Nerves. (After Henle.) 
ci, internal carotid. H, pituitary body. /, part of tentorium, fcb., falx cerebelli. 



the anterior central convolution, and it is very probable that 
injury to this region causes a motor disturbance in the tongue. 
A priori, no objection can be made to this conclusion; a poste- 
riori, it has not yet been confirmed, as proofs from autopsies 
are still wanting. It is impossible, therefore, to make even a 



DISEASES OF THE HYPOGLOSSAL NERVE. 



145 



surmise with regard to the relative frequency (or rather infre- 
quency) of the affection. 

The bulbar lesion of the nerve or rather its nucleus is some- 



Fissure of Rolando 

Parietal lobe 



Pa rieto-occipital 
fissure 




Fig. 30.— Cortical Centres of the Left Hemisphere. (After Gowers.) 



what better understood; it has undoubtedly been observed, if 
not frequently, at least repeatedly, that this lesion can occur 




Fig. 31. — Cross-section through the Medulla Oblongata. (After Wernicke.) 
12, root-fibres of the hypoglossal nerve. X.a., nucleus ambiguus (anterior vagus nu- 
cleus). X, posterior vagus nucleus. X.f., common root of the "mixed lateral system." 
8. <?., external, 8. z'., internal auditory nucleus, ci, restiform body, oi, olive. V. a., as- 
cending root of the trigeminus, p., pyramid. 



unilaterally. There is then an atrophy of the nucleus, in 
which the ganglionic cells and the medullated fibres become 



146 



DISEASES OF THE CRANIAL NERVES. 



decreased in number or disappear entirely, while the roots 
appear as fine threads. In such cases (see especially Fig. 32) 
the tongue is protruded, not straight, but deviates toward one 
side, and be it remembered toward the affected side (m. genio- 
glossus and geniohyoideus) ; it shows fibrillary twitchings, and 
an atrophy of the diseased side — hemiatrophia linguae — which 




Fig. 32.— Hemiatrophia Linguae (personal observation). 



in such a case looks flabby and shrunken in comparison with the 
full and firm healthy half; it is wrinkled, contracted, and much 
smaller than the latter (cf. Figs. 32 and 33, showing my two 
cases). The electrical examination shows either normal reac- 
tion or reaction of degeneration ; that the latter may also 
occur in central lesions has been demonstrated by one of my 
cases, which, however, did not come to autopsy. Speech, 
mastication, and deglutition often suffer considerably ; on the 
other hand, the healthy half of the tongue may develop so sat- 
isfactory and vicarious an activity that little disturbance is 
observable. 



DISEASES OF THE HYPOGLOSSAL NERVE. 



H7 



Unilateral paralysis of the hypoglossal nerve has been ob- 
served as a result of traumatism ; further, also, in diseases of 
the vertebral artery, as the result of new growths in the me- 
dulla oblongata and in cases of embolic softening in the region 
of the nucleus (Hirt). Whether it can be also of saturnine 
origin seems to me to be doubtful, in spite of the report of 




Fig- 33.— Hemiatrophy Lingua (personal observation). 

Remak. In a recently published article by Koch and Marie 
(cf. lit.) may be found all the cases observed up to the present 
time collected and minutely analyzed. 

In bilateral paralysis of the hypoglossal the tongue, atrophic, 
wrinkled, and shrunken, lies almost motionless on the floor of 
the mouth ; the patient can not protrude it, and has entirely 
lost control over it. Speaking and chewing are rendered diffi- 
cult, even quite impossible. This sad picture is seen not infre- 
quently in Duchenne's progressive bulbar paralysis, occasionally 
in progressive muscular atrophy, very rarely in tabes. The 
hemiatrophy of the tongue, too, occurs much less frequently in 
the course of tabes than, to judge from the communications — 



I4 8 DISEASES OF THE CRANIAL NERVES. 

for instance, those of Ballet (cf. lit.) — would seem to be the 
case. 

The peripheral form of the affection may yield to electrical 
treatment (faradization and galvanization) ; the central, as far 
as we know at present, is not amenable to any treatment. 

Hypoglossal spasm occurs sometimes unilaterally, some- 
what more frequently bilaterally. It is an exceedingly rare 
affection, in regard to which there have been but few good 
publications. There is a paroxysmal, involuntary spasm of the 
tongue, by which it is protruded and retracted, rolled violently 
around in the mouth, and so roughly pressed against the teeth 
that it may be quite severely injured. In some instances there 
occur short rhythmical twitchings in the whole tongue which 
disappear at times. Berger observed an aura before such an 
attack, which consisted in a sensation of tension and swelling 
of the tongue. In Dochmann's case the attacks occurred espe- 
cially at night, and were so violent that the patient, a woman, 
was waked up by the sudden spasmodic protrusion of the 
tongue. In one of my own cases the muscles of mastication 
took part in the affection in such a way that before the actual 
hypoglossal spasm occurred, the lower jaw was for a half or a 
whole minute spasmodically jerked to and fro, up and down. 
After these movements had ceased the mouth remained half 
open, and the turning and rolling movements of the tongue 
commenced and lasted for about one minute. These attacks 
recurred ten to twenty times a day ; they came on for the first 
time three days after an epileptic fit, and have lasted unaltered 
ever since (for three years). The patient is otherwise perfectly 
healthy, and has a good family history. The pathogenesis of 
the disease, its anatomical seat (irritation of the hypoglossus 
centre? cortical or bulbar?), is obscure. As an accompanying 
symptom of chorea and Irysteria it is by far more common than 
as an independent affection. The treatment is the same here 
as in paralysis of the tongue. 

LITERATURE. 
I. Paralysis of the Hypoglossal Nerve. Hemiatrophia Ungues. 

Fairlie-Clarke. A Treatise on the Diseases of the Tongue. London, 1873. 
Moser. Beitrag zur Diagnostik der Lage und Beschaffenheit von Krankheits- 

herden der Oblongata. Deutsches Arch. f. klin. Med., xxxv, p. 418, 1884. 
Ballet. De l'hemiatrophie de la langue. Arch, de Neurol., vii, 20, 1884. 
Hirt. Ueber Hemiatrophie der Zunge. Berl. klin. Wochenschr., No. 25, 18S5. 



DISEASES OF THE HYPOGLOSSAL NERVE. 



[49 



Erb. Ein seltener Fall von atrophischer Lahmung der N. hypogl. Deutsches 

Arch. f. klin. Med., xxxvii, p. 265, 1885. 
Schiffers. De 1 hemiatrophie de la langue. Revue mens, de laryngologie, 

d'otologie, et de rhinologie. 
Remak, E. Ueber saturnine Hemiatrophie der Zunge. Berl. klin. Wochen- 

schr., xxiii, 25, 1886. 
Sauer. Fall von traumat. Hypoglossus- u. Accessoriuslahmung. Inaug. Diss. 

Gdttingen, 1886. (Unilateral luxation between atlas and epistropheus.) 
Peel. Berl. klin. Wochenschr., No. 29, 1887. (Hemiatrophy of tongue, with 

left-sided recurrens paralysis.) 
Koch et Marie. Hemiatrophie de la langue. Revue de med., viii, 1, 1888. 

2. Hypoglossal Spasm. 

Berger. Ueber idiopathischen Zungenkrampf. Neurol. Centralbl., i, 3, 1882. 

Dochmann. Petersb. med. Wochenschr., 1, 1883. 

Wendt. Unilateral spasm of the tongue. Americ. Journ. of Med. Sc, clxxvii, 

p. 173, Jan., 1885. 
Erlenmeyer. Centralbl. f. Nervenheilk., ix, No. 5, 1886. (Case of idiopathic 

spasm of the tongue.) 
Bernhardt. Ueber idiopathischen Zungenkrampf. Ibid., No. 11, 1886. 



CHAPTER XI. 

SIMULTANEOUS AFFECTION OF SEVERAL CRANIAL NERVES MULTIPLE 

PARALYSIS OF THE CRANIAL NERVES. 

After having thus considered the lesions of the individual 
cranial nerves, it remains for us to inquire under what condi- 
tions several of them may be simultaneously affected, and into 
the symptoms thus produced. According to the observations 
collected up to the present time, an affection of this kind may 
have its seat in the peripheral or in the central course of the 
nerves, as well as in the cortical or nuclear centres. Only cer- 
tain of the affections of this latter kind are to be regarded as 
independent diseases, while the peripheral lesions are always 
only partial manifestations of other diseases. In rare cases 
a simultaneous peripheral lesion of several cranial nerves may 
occur in consequence of traumatism, operative interferences, 
etc. A case in point, in a patient operated upon by Israel, has 
been published by, Remak (Berl. klin. Wochenschr., 7, 1888). A 
cavernoma of the neck was extirpated, and by the operation 
the accessorius, the hypoglossus, and the sympatheticus were 
injured, or rather resected. The symptoms caused by the acci- 
dent were accurately described by Remak. Other instructive 
cases, due to traumatism, have been described by Mobius (cf. lit.). 

Among the general diseases in which multiple cranial nerve 
lesions may occur are chiefly tuberculosis and syphilis. 

Tubercular meningitis attacks, by preference, the mem- 
branes at the base, and implicates most of the cranial nerves 
emerging in that region, as we have seen in our account of the 
diseases of the meninges. Lately Kahler (cf. lit.) has again 
directed attention to the fact that, in consequence of syphilis, 
a peripheral neuritis of the cranial nerves sometimes develops, 
and that we may, besides general cerebral symptoms, have a 
progressive slow paralysis, which attacks one cranial nerve 
after the other in irregular succession. 



POST-DIPHTHERITIC PARALYSIS. 



151 



After diphtheria peculiar forms of paralysis are observed, 
which chiefly take in the muscles of the soft palate and the 
pharynx. Since these muscles are innervated by certain of 
the cranial nerves, and the disease is unquestionably — e. g., 
when the paralysis is unilateral — often of peripheral origin (cen- 
tral diseases can not in all other cases be excluded), we shall 
devote a few lines to the consideration of their nerve supply. 

The innervation of the palatal and pharyngeal muscles is by no 
means one of the clearest chapters in neurology. We do not know 
exactly which of the cranial nerves are concerned, nor their mode of 
distribution. Of the palatal muscles the levator palati is the most 
important. This receives motor fibres through the large superficial 
petrosal (of the trigeminus) from the spheno-palatine ganglion, which 
come from the facial and which also innervate the azygos uvulae. 
Whether or not, however, the vago-accessorius and the glosso-phar- 
yngeus are also concerned in the innervation of these muscles, as 
Gowers, for instance, seems to think, basing his arguments upon 
clinical observations, is not as yet decided (cf. page 85). With regard 
to the pharyngeal muscles, it is generally assumed that the stylo- 
pharyngeus and the middle constrictor are supplied by the glosso- 
pharyngeal nerve, and that the palato-pharyngeus, the superior and 
inferior constrictors, are innervated by the vagus. The participation 
of the accessorius is doubtful (Schwalbe). We see then that the nerves 
concerned in a paralysis of the pharynx are the facial, the glosso- 
pharyngeal, the vagus, possibly also the fifth and the accessorius. 

Pharyngeal paralysis may be either unilateral or bilateral. 
The unilateral form can only be diagnosticated if the patient is 
made to move the soft palate, for instance, in saying "Ah!" 
While during rest it appears to be perfectly symmetrical, the 
base of the uvula deviates somewhat on motion towards the 
affected side, so that on that side a little way from the median 
line there is a slight depression not present on the well side ; 
sometimes also the soft palate is a little lower on the para- 
lyzed side even during rest. In the bilateral complete paralysis 
of the soft palate, the latter hangs down flaccidly and the uvula 
appears elongated ; on deep respiration and on phonation it 
remains motionless, and the reflex movements evoked by tick- 
ling the mucous membrane are lost. Speech becomes mark- 
edly altered, the voice acquires a nasal tone, due, of course, to 
the cavity of the nose not being shut off during phonation ; 
hence also the pronunciation of the explosive consonants " P " 
and " B " becomes impossible, owing to the imperfect com- 



DISEASES OF THE CRANIAL NERVES. 



pression of the air ; they sound like " M." Closure of the an- 
terior nares removes, as Duchenne has shown, this disability. 
From the same cause also fluids are re- 
gurgitated through the nose on attempts 
at swallowing, and deglutition in gen- 
eral becomes difficult. 

The prognosis in post-diphtheritic 
paralysis is not unfavorable if the velum 
palati alone is paralyzed. If, on the 
other hand, the muscles of the oesopha- 
gus also take part, the outlook becomes 
graver on account of the inability of 
the patient to take nourishment, and all 
the more so if feeding by the stomach- 
tube is not constantly and carefully 
practiced. If this is not done, aspira- 
tion pneumonia or inanition may bring 
about a fatal issue. 

The electrical treatment ought to be 
begun as early as possible. It consists 
in the direct faradization or galvaniza- 
tion of the velum and the frequent ex- 
citation of reflex movements of deglu- 
tition by stimulation of the throat. The 
uvula, the pillars of the pharynx, etc., 
are directly touched and repeatedly 
stimulated by means of the curved but- 
ton electrode (cf. Fig. 34). The move- 
ments of deglutition are obtained if the 
anode is placed on the neck and the 
cathode (button electrode) is quickly 
drawn over one of the lateral surfaces 
of the larynx, six to ten cells sufficing 
for the purpose. These gymnastics of 
the pharyngeal muscles constitute an 
excellent remedy which can not be re- 
placed by any other. It often leads 
rapidly to recovery. 
Central diseases of several cranial nerves at the same time 
may also occur, and that, too, not only in their intracerebral 
course — which for but few of them is known, and for those 
only imperfectly — but also in the centres themselves. As a 




Fig. 34.— Pharyngeal and La- 
ryngeal Electrode with 
Arrangement for making 
and breaking the cur- 
RENT. (After Erb.) 



POLIOENCEPHALITIS {WERNICKE). 



153 



matter of fact, our knowledge about the centres situated in the 
cortex is also very incomplete, since we must again confess our 
comparative ignorance of the anatomy. Still, we shall not go 
too far if we assume that extensive cortical lesions may impli- 
cate several centres together, and there is no doubt but that 
they may be affected after or rather during an apoplectic at- 
tack by " indirect action." 

Of eminently practical importance are the nuclear affections 
of the cranial nerves. Referring the reader to the preceding 
chapters for the anatomical position of the individual nuclei, 
we will only remind him of the fact that these nuclei are situ- 
ated in the gray matter, partly of the mid- and 'tween brain, 
partly in the medulla oblongata. The portion situated above 
the latter extends from the posterior wall of the infundibulum 
in the third ventricle to the level of the nucleus of the abdu- 
cens, and embraces the nuclei of the eye muscles (Wernicke). 
The other nuclei belong to the lower portion. 

Clinical observations now teach us that either of these por- 
tions may be affected by itself, and we may with Wernicke call 
the disease of the upper, polioencephalitis superior ; that of the 
lower, polioencephalitis inferior. According to the course, we 
distinguish in either case an acute and a chronic form, so that 
there are altogether four clinical pictures of these nuclear af- 
fections. 

Polioencephalitis superior acuta has only been observed in 
very few instances. The best observations we owe to Wernicke. 
According to him, this is essentially an acute inflammatory dis- 
ease of the nuclei of the ocular muscles, and proves fatal in 
from ten days to a fortnight, the focal symptoms consisting in 
an associated paralysis of the eye muscles, the general symp- 
toms being grave disturbances of consciousness. The walk 
presents a peculiar combination of spasm and ataxia. Anatom- 
ically, foci of acute softening are found in the region of the 
nuclei, which are either due to obstruction of the blood-vessels 
or to inflammatory infiltration of the tissues. ^Etiologically, 
the abuse of alcohol may be mentioned. 

Polioencephalitis inferior acuta (acute bulbar paralysis, acute 
bulbar myelitis) is also an extremely rare affection. It is equal- 
ly rapidly fatal after the quick development of all those symp- 
toms which we shall describe shortly in our account of chronic 
bulbar paralysis. Microscopically, inflammatory changes are 
found in the lower nuclear region. 



154 



DISEASES OF THE CRANIAL NERVES. 



Polioencephalitis superior chronica was described in 1868 
by von Graefe, and called by him ophthalmoplegia progressiva. 
The first published case presented, according to von Graefe 
(Berl. klin. Wochenschr., n, 1868), a peculiar clinical picture: 

" Gradually all the muscles concerned in the movements of 
the eye become paralyzed, causing first a diminution in the 
range of sight, and finally resulting in complete immobility of 
the eyeballs. The levator palpebral superioris is wont to be 
implicated, although the consequent ptosis is rarely as marked 
as that occurring in complete oculo-motor paralysis. It is re- 
markable that, on examination for reaction to light and accom- 
modation, the sphincter pupillas as well as the ciliary muscle 
present no changes. This condition, which we very rarely 
find in other extensive oculomotor paralyses, seems here con- 
stant and characteristic of this disease. Another feature which 
distinguishes this form from other associated paralyses in the 
distribution of the third, fourth, and sixth nerves is the prog- 
ress of the disease pari passu in the antagonizing muscles. 
Thus we never find a marked strabismus divergens owing to 
a dominating oculo-motor paralysis, because here the external 
rectus loses its functions sufficiently to neutralize the tendency 
to deviation, and the sight of the patient is therefore, in spite 
of the associated paralysis of the eye muscles, affected much 
less than in simple oculo-motor or abducens paralysis. . . . 
Still, a certain degree of asymmetry in the affection of the dif- 
ferent muscles of one eye, as well as in the development of the 
whole disease in the two eyes, may at times be found." (Cf. 
Wernicke, Ivc. cit., vol. iii, page 463.) 

With the exception of this associated ocular palsy, which, 
developing progressively, may remain stationary without being 
completely symmetrical, the patient enjoys good health and 
complains neither of headache nor of symptoms of increased 
intracranial pressure. In isolated instances bulbar paralysis 
has been known to be later superadded, and in others the dis- 
ease was complicated by multiple sclerosis. Anatomically, the 
affection depends either upon a primary disease of the nuclei of 
the ganglionic cells or upon a diffuse sclerotic process in which 
the nuclei of the nerves take part. In exceptional cases, which 
in their nature are as yet entirely obscure, no organic changes 
whatever have been found, although the clinical picture corre- 
sponded exactly to that described by von Graefe. (Eisenlohr 
and Oppenheim.) 



BULBAR PARALYSIS. 



155 



Not less interesting, and at the same time of by far greater 
practical importance because relatively far more frequently 
met with, is the fourth and last of the affections under consid- 
eration — a disease the first accurate description of which we 
owe to Duchenne, of Boulogne, and which after him has been 
carefully and successfully studied by German investigators 
(Wachsmuth, Kussmaul, Leyden) — the chronic progressive bul- 
bar paralysis. 

Progressive Bulbar Paralysis. 

Paralysis of the Tongue, the Soft Palate, and the Lips {Duchenne, i860), Glosso-labial 
Laryngeal Paralysis { Trousseaii), Chronic Progressive Bulbar Paralysis ( Wachs- 
muth, 1864), Atrophic Bulbar Paralysis {Leyden), Bulbar Nuclear Paralysis {Kuss- 
maul), Polioencephalitis Lnferior Chronica { Wernicke). 

Duchenne s Disease. 

Symptoms and Course. — In the majority of instances the 
onset of progressive bulbar paralysis is very gradual, and only 
rarely do we meet with cases in which it is ushered in by an 
apoplectiform attack. After having complained for weeks, 
perhaps months, of drawing, tearing pains in the neck and the 
back, the patient discovers of his own accord or from the re- 
marks of his relatives that the enunciation of certain words, 
especially those containing /, r, and long e, has become very dif- 
ficult. If he happen to use a word containing all these letters 
(for instance, reel), he becomes painfully conscious of his indis- 
tinct enunciation. In vain he attempts to repeat the trouble- 
some words over and over again in order to correct his mis- 
take. He only becomes more convinced that the movements of 
his tongue have become clumsy, and that he has lost his for- 
mer ease and fluency of speech ; and, in truth, it is the on- 
coming paresis of the lingual muscles which is the main cause 
of the disturbance. 

The tongue, which can not be raised to the normal extent, 
can no longer be approached sufficiently to the hard palate, 
and thus the 1.0 ng e, for the pronunciation of which the move- 
ment is necessary, can only be pronounced with difficulty. In 
the same way all the finer muscular movements required for 
the formation of the Unguals are imperfect, and consequently 
the enunciation of these sounds is bad. The disease progresses 
and the articulation becomes worse and worse, the less per- 
fectly the lingual muscles are innervated, and other letters, 
s, t, g, finally also d and n, begin to suffer, so that conversation 



i 5 6 



DISEASES OF THE CRANIAL NERVES. 



with the patient becomes very uncomfortable, as certain words 
are almost unintelligible and others at least difficult to under- 
stand. 

The lips also begin to do their duty badly, so that the enun- 
ciation of the so-called labials — o, u, a, b, p — gradually becomes 
indistinct. The presence of strangers with whom he has to 
converse excites the patient, and, avoiding all society, he pre- 
fers the quiet 
monotony of 
the family cir- 
cle, where no- 
body seems to 
pay much at- 
tention to the 
change in his 
speech ("ala- 
lia and anar- 
thria "). More- 
over, a change 
in the features 
of his face, at 
first slight and 
only noticed 
by the patient 
himself, but 
later more per- 
ceptible and 
evident also 
to his friends, 
gradually man- 
ifests itself, 
which serves 
as an addition- 
al reason for 
seclusion (Fig. 35). When laughing, it appears to him as if 
a certain tension in his lips prevented the usual play of the 
mouth. In the attempt to whistle the lips can not be puckered 
as well as formerly ; the muscles of the cheek have become 
more rigid and inactive, and as the disease progresses the 
whole lower half of the face assumes a characteristic appear- 
ance — a peculiar lachrymose and astonished expression — which, 
as is easily seen, is due to the drooping of the lower lip and to 




Fig. 35- 



-Facial Expression in Progressive Bulbar Paraly- 
sis. ( After Leyden, Eichhorst.) 



BULBAR PARALYSIS. 



157 



the deepening of the naso-labial fold. The upper half of the 
face, the forehead and eyes, do not take part in the change, 
but remain entirely normal. Nevertheless the patient's face is 
much disfigured, and later on in the disease may have become 
almost unrecognizable. 

While thus quite gradually symptoms have arisen which 
make the patient a very pitiable object, and which are bound 
sooner or later to interfere wiLh his position in society, the sad 
truth dawns upon him that even the functions absolutely neces- 
sary for the existence of life are failing. Eating, in which up 
to this time no trouble was experienced, he now finds difficult. 
It takes a longer time to swallow the food, and in a later stage 
even mastication becomes impaired. Not only do the move- 
ments of the lower jaw become weaker and less energetic, 
owing to paresis of the muscles of mastication, but, since the 
powerless tongue is unable to get the food from between the 
cheeks and gums into the region of the pharyngeal muscles, 
the formation of the bolus is impossible. Spoons, fingers, and 
the like, have to be used instead, or the patient has to hold his 
head far back to get the food to slide down. Even drinking 
causes much discomfort, as the liquid may get into the larynx 
and thus give rise to violent coughing, or may be regurgi- 
tated through the nose, either condition being due to weak- 
ness of the pharyngeal and laryngeal muscles. 

The implication of the larynx is very distressing, and may 
indeed become dangerous. The voice at times fails, speech 
becomes irksome, and the tone is monotonous ; production of 
the higher notes as in singing becomes impossible ; later on a 
marked hoarseness and finallv aphonia follows, so that the pa- 
tient can only express himself in whispers, which, owing to the 
above-described motor changes, are quite unintelligible. At 
the same time the absence of a firm closure of the glottis, and 
therefore the inability to cough forcibly, gives rise to various 
disturbances in the respiratory apparatus, owing to the disa- 
bility to dislodge mucoid masses which may have collected in 
the air passages. 

Another symptom which, though not constant, is frequently 
met with is the marked increase in the secretion of the saliva. 
This occurs usually rather early in the disease, and not infre- 
quently such patients are seen going around constantly holding 
their handkerchiefs to the mouth to prevent the saliva from 
trickling away. On examination, the secretion is found to be 



i 5 8 



DISEASES OF THE CRANIAL NERVES. 



viscid. This flow of saliva is due to an actual increase in the 
amount secreted, as several careful investigators have shown, 
though they do not agree as to the exact amount. 

Two, three, even five years may pass before any new symp- 
toms are added to those just described. These, however, pro- 
gressively gain in intensity, and it is especially the change in 
the features which becomes more accentuated, owing to the 
constantly increasing atrophy in the muscles of the lips and the 
cheeks; the palatal reflexes become markedly decreased and 
finally lost ; the tongue, shrunken and distinctly smaller, lies 
immobile on the floor of the mouth, and can neither be pro- 
truded nor moved in any direction. Fibrillary tremor is then 
not uncommonly marked. On the electrical examination 
(which is, by the way, very hard to make), we may find reac- 
tion of degeneration in the lingual as well as in the pharyngeal 
muscles (cf. page 146). 

The inability to take food properly is usually the cause of 
death ; the patient pines away, and gradually dies from inani- 
tion without having: the blissful benefit of a dulled conscious- 




36.— Cross-section through the Upper Portion of the Medulla Oblon- 
gata. On the left the healthy, on the right the diseased medulla, hk on the left the 
normal, hk on the right the diseased hypoglossus nucleus (the ganglionic cells are almost 
entirely absent on the right side). 

ness to guide him insensibly through his tormenting sufferings. 
Only in occasional instances disease of the respiratory organs, 
caused by aspiration of food, hastens the termination (aspira- 
tion pneumonia). 



BULBAR PARALYSIS. 



159 



Pathological Anatomy. — There is hardly another disease of 
the nervous system with the anatomical basis of which we 
are better acquainted than bulbar paralysis. Duchenne pro- 
nounced the process to be a primary pigmentary degenera- 
tion, and atrophy of the large ganglionic cells in the nuclei of 
the medulla oblongata, an assertion which has received com- 
plete confirmation from all subsequent investigators. Micro- 
scopical examination shows atrophy of the ganglionic cells. 
This is shown in Fig. 36 in the nucleus of the hypoglossal ; the 
cells have in this case completely disappeared, having previ- 
ously diminished in size and 
lost their processes. At the 
same time we find the con- 
nective tissue increased, the 
walls of the vessels in the 
nucleus thickened. Similar 
changes are found in the nu- 
cleus of the vagus accessory 
and the glosso- pharyngeal 
nerves (the so-called lateral 
mixed system, cf. page 95). 
Since, as we have said before, 
the upper part of the face 
always remains normal dur- 
ing the disease, we have to 
assume that the fibres inner- 
vating these muscles arise 
from a special centre. This 
is supposed to be a part of 
the abductor nucleus (Mey- 
nert), which has therefore 
come to be designated by 
the composite name of fa- 
cial-abducens nucleus. (For 
the position of the nuclei, 
cf. pages 42 and 77.) This and the remaining nuclei, with the 
exception of those mentioned above, were always found to 
be intact. The atrophy also extends to the root fibres, which, 
to the naked eye, often appear smaller and of a grayish color. 
From the topographical position of the nuclei below the floor 
of the fourth ventricle, as it is approximately represented in 
Fig". 37, we can easily understand how, on the one hand, the 




Fig- 37-— The Posterior (Dorsal) Aspect 
of the Medulla Oblongata, i, poste- 
rior commissure. 2, peduncle of pineal gland. 
3, corpora quadrigemina. 4, superior pedun- 
cle. 5, middle peduncle. 6, inferior pedun- 
cle of cerebellum. 7, stria acusticse. 8, funic, 
teres. 9, obex. 10, funicul. gracil. 



l6o DISEASES OF THE CRANIAL NERVES. 

pathological process, after having attacked the hypoglossus, 
next implicates the neighboring vagus, and, on the other hand, 
how the motor part of the trigeminus usually remains unaf- 
fected, so that paralysis of the muscles of mastication is very 
rare. But why the auditory is constantly exempt and the 
facial partially affected are circumstances which need to be 
further investigated. A complete counterpart to bulbar paral- 
ysis is found in the so-called progressive muscular atrophy, a 
disease in which, as we shall see later on, the gray anterior 
horns of the spinal cord and their ganglionic cells are affected 
precisely in the same way as the bulbar nuclei in the disease 
we are now discussing. The ganglionic cells of the anterior 
horns constitute the trophokinetic centres for the muscles sup- 
plied by the spinal nerves, an office which the bulbar nuclei 
fulfill for those supplied by the cranial nerves. In both dis- 
eases there is atrophy and decrease in the functional power, 
and in both the disturbance is strictly motor, while sensation is 
absolutely intact. This essential similarity between the two 
diseases explains why not rarely one is associated with the 
other — in other words, why they may complicate each other. 
We may, indeed we frequently do, meet with cases in which 
bulbar paralysis is accompanied by atrophy of the muscles of 
the extremities, while, on the other hand, in progressive mus- 
cular atrophy, bulbar symptoms, disturbances in deglutition 
and speech, may be found. 

Another analogy exists between bulbar paralysis and amyo- 
trophic lateral sclerosis, a disease in which not only the gan- 
glionic cells of the anterior gray horns, but also the motor 
tract in the lateral columns of the spinal cord is affected. All 
these diseases, viewed from an anatomical standpoint, if not 
identical, certainly are closely related to each other, and only 
differ in the position of the lesions ; it is, therefore, advisable 
to consider and study them from a common point of view, 
as the understanding of the individual symptoms will thus be 
much less difficult. 

Diagnosis. — As to the diagnosis, we need not be doubtful if 
we always remember that the disturbances are confined to the 
motor functions of the nerves governing the muscles of the 
lips, tongue, pharynx, and larynx, to which disturbances all the 
symptoms described above may be attributed. If we find any 
well-marked sensory changes, if the patient complains of pain 
or paresthesias and the like, we either have to give up the 



BULBAR PARALYSIS. j6i 

diagnosis of bulbar paralysis, or we have to search for some 
complication. The peculiar facial expression, the increased 
flow of saliva, the tremulous atrophic tongue partially or even 
completely immobile as it is, the disturbance in speech and 
deglutition, when taken together are so characteristic that, if 
intelligently observed and studied, they will make our diag- 
nosis clear. 

There is only one case in which we may be doubtful ; cer- 
tain foci of disease in the brain may produce symptoms simu- 
lating bulbar paralysis, so much so indeed that the name pseudo- 
bulbar paralysis has been given to the condition (which later on 
will be described more at length) ; nevertheless, with due care- 
fulness we can avoid a mistake. The most important point to 
observe in the differential diagnosis is the course of the disease. 
While in progressive chronic bulbar paralysis this is slow, but 
always progressive toward the fatal end, in the spurious form 
remissions may occur, so that for years the patient may be im- 
proved, though he finally also succumbs to the disease. Besides 
this, pseudo-bulbar paralysis is often attended with cerebral 
symptoms, headache, apoplectiform attacks, etc. More about 
this will be found under the head of pathological diagnosis in 
the chapter on encephalo-malacia. 

Prognosis. — The prognosis, as we should expect after what 
has been said, is altogether unfavorable. There is, according 
to our present knowledge, no cure for the true bulbar paralysis, 
and one ought to be careful, therefore, not to deceive the family 
with promises. As soon as the diagnosis is made they ought 
to be informed of the unfavorable outlook. 

Treatment. — The only treatment from which any success 
may be expected, if begun early, is the systematic use of elec- 
tricity : faradization and galvanization of the threatened mus- 
cles, especially of those of the tongue and pharynx, frequent 
excitation of the movements of deglutition, according to the 
method described on pages 151 and 152, are the only measures 
which deserve confidence. With the exception of this local 
treatment, there is nothing that affords even a temporary bene- 
fit. I have never seen any lasting effect from hydrotherapy, 
but still this treatment is very frequently advised just at that 
stage of the disease when electricity might do some good. 
Internal remedies are of no avail ; the occasional symptomatic 
use of atropine ( T / 2 to 1 milligramme (Y I20 to J / 6o gr.) daily) to 
diminish the salivary secretion may be indicated. It scarcely 



^2 DISEASES OF THE CRANIAL NERVES. 

needs to be mentioned that the chief duty of the physician in 
the later stages of the disease is to pay the most careful atten- 
tion to the general nutrition of the patient. 

./Etiology. — The aetiology is still obscure. It is true that 
there are patients affected with the disease who, owing to their 
occupation, have made rather excessive use of the muscles of the 
tongue and palate (glass-blowers, musicians). These cases, how- 
ever, are so rare that it would seem very forced to attribute any 
^etiological importance to this factor. The same may be said 
about syphilis, the truth being that, in most cases, the cause is 
absolutely obscure, and all we can say is that males and persons 
advanced in life seem to be more frequently attacked by the 
disease than others. Heredity but rarely plays a part, and the 
influence of cold remains, in connection with this disease, as 
obscure as with all other nervous affections. 

LITERATURE. 

Bourdon. Gaz. hebdom., 2me seY, ix, 22, 1872. (Assumes three groups of dis- 
eases of the medulla : those of the anterior, middle, and posterior portions.) 

Leyden. Klinik der Ruckenmarkskrankheiten. Berlin, 1875, ii, 427 et seq. 

Hallopeau. Des paralysies bulbaires. Paris, 1875. 

Kayser. Zur Lehre von der progressiven Bulbarparalyse. Inaug. Diss. Ber- 
lin, 1876. 

Wernicke. Loc. cit., iii, pp. 470 et seq., 1883. 

Mobius. Ueber mehrfache Hirnnervenlahmung. Erlenmeyer'sches Centralbl. 
f. Nervenheilk., x, 15, 16, 1887. 

Kahler. Die multiple syphilitische Wurzelneuritis. Zeitschr. f. Heilk., viii, 1. 
Heft, 1, 1887. 

Thomsen. Ueber eigenthiimliche, aus veranderten Ganglienzellen hervorge- 
gangene Gebilde in den Stammen der Hirnnerven des Menschen. Virchow's 
Arch., Bd. 109, p. 459, 1887. 

Eisenlohr. Fall von Ophthalmoplegia ext. progressiva mit bulbaren Sympto- 
men ohne Befund. Aerztl. Verein zu Hamburg. Sitzung vom 19. April 
1887. Deutsche med. Wochenschr., No. 32, 1887. 

Striimpell. Loc. cit., pp. 283 et seq., 1887. 

Eichhorst. Loc. cit., p. 316, 1887. 

Dutil. Gaz. des Hop , No. 34, p. 399, 1887. 

Oppenheim and Siemerling. Die acute Bulbarparalyse und die Pseudobulbar- 
paralyse. Charite-Annalen, xii, 1S87. 

Unverricht. Ueber multiple Hirnnervenlahmung. Fortschr. d. Med , 24, 1887. 

Pel. Berl. klin. Wochenschr., xxiv, 29, 1887. 

Mobius. Centralbl. f. Nervenheilk., x, 15, 16, 1887. 

Ziemssen, v. Ueber diphtherische Lahmungen u. deren Behandlung. Leipzig, 
Vogel, 1887. 

Semmola. Ueber die paralytische Herzataxie bulbaren Ursprungs. Prag. med. 
Wochenschr., 9, 1887. 



PART III. 

DISEASES OF THE BRAIN PROPER. 

When we have reason to suspect a brain lesion in a patient, 
the questions which arise are : (i) Where is the seat of the 
lesion? (2) What is its pathological nature? To the physician 
both of these questions are of interest ; to the patient, more 
especially the latter. 

The examination which searches for the seat of the lesion 
will give us the topical diagnosis (ro7ro<; = place) ; the exam- 
ination concerning the nature of the lesion, the pathological 
diagnosis. 

The endeavor to localize cerebral lesions — that is, to make 
a topical diagnosis — has only of comparatively late years re- 
ceived attention, and much of the work so far done can not be 
called more than an attempt, in many cases indeed only a weak 
one. The celebrated discovery of Broca (1861), that certain 
disturbances of speech were often found associated with lesions 
in the third left frontal convolution, the discovery of Fritsch 
and Hitzig (1870), that stimulation of certain areas of the cortex 
produces contractions in certain definite groups. of muscles on 
the opposite side of the body — these and various other, patho- 
logical, observations, to which reference will be made later, 
make it most probable, nay, almost certain, that definite parts 
or areas of the cortex are always connected with certain func- 
tions of the brain ; in other words, that these functions can be 
localized ; and, notwithstanding the many uncertainties and 
numerous contradictions between the results of experiments 
on the one hand and those obtained from clinical observations 
on the other, it is this doctrine of cerebral localization which, 
though still undeveloped, must be considered as the basis of 
all further investigation in the field of cerebral pathology. 

Equal stress must, however, be laid upon the examination 
into the nature of the lesion. A certain symptom — for instance, 



164 DISEASES OF THE BRAIN PROPER. 

a persistent hemiplegia — is always the result of a lesion of the 
motor tract ; a lesion, however, which can be produced in 
quite a variety of ways. It may be due to cerebral haemor- 
rhage, to a tumor, an abscess, etc. It is therefore, especially 
with regard to the prognosis, of the greatest importance to 
determine the exact nature of the lesion in a given case, but 
both questions ought always to be investigated with equal 
care if we wish to arrive at as exact a diagnosis as circum- 
stances permit. In the following pages these two modes of 
diagnosis will be considered separately, and we shall first speak 
of what is known about cerebral localization, while in a later 
chapter the pathological side will be discussed. 

I. The Study of Cerebral Lesions with Reference to 

their Seat — Topical Diagnosis — Doctrine of 

Localization. 

Two classes of symptoms produced by cerebral lesions 
must be distinguished — first, general or diffuse (Griesinger) ; 
and, secondly, local. The former, so far as they concern the 
subjective feelings of the patient and the disturbances of the 
vegetative functions (temperature, pulse, respiration, condi- 
tion of urine), are to be observed and described in this con- 
nection in the same way as in diseases of other organs. The 
latter — the local symptoms — may be divided into two classes 
— namely, the direct and the indirect. We call those symp- 
toms direct which are produced by a persistent disturbance in 
the functions of a certain part of the brain. They are also 
called focal symptoms (Griesinger). By indirect symptoms we 
mean those which are only produced by transient conditions 
— changes in circulation, by compression, etc., and which are 
in a way concomitant symptoms of the former. They may be 
entirely absent ; on the other hand, they may be so prominent 
as to make a topical diagnosis impossible. 

Destruction of a circumscribed area in the brain gives rise 
to symptoms of paralysis, or less frequently to symptoms of 
irritation. The former, where we have to deal with a loss of 
function, are also (after Goltz) called symptoms of destruction 
(Ausfallssymptome), and if the function is not lost but is only 
impaired, symptoms of impairment [Hemmungssymptome). The 
latter — namely, the irritative symptoms — are usually due to a 
so-called indirect action. 

It is not always possible to say whether a symptom is of a 



CEREBRAL LOCALIZATION. jg- 

direct or of an indirect nature. For instance, if we find a pa- 
tient in an unconscious state with a hemiplegia, this hemiplegia 
may be a direct focal symptom or it may have been produced 
indirectly. In the latter case it will disappear in a few hours or 
days, in the former it will be persistent. Or, if a patient suffer- 
ing from the consequences of a cerebral haemorrhage presents, 
as is often the case, disturbances in speech, this may again 
be a focal symptom or not. If, after consciousness has been 
regained, the speech becomes gradually but steadily better, 
then the aphasia was produced indirectly. If, however, speech 
remains unintelligible for months or years, it is clear that we 
have to do with a focal symptom. Therefore, in acute lesions 
we can only after a certain time has elapsed discriminate be- 
tween direct and indirect symptoms. 

The irritative symptoms consist either of general epilepti- 
form convulsions or of partial, involuntary movements of the 
extremities (hemichorea, athetosis), of tremors, contractures, or 
forced movements of the whole body. We shall repeatedly 
have occasion to refer to these phenomena. 

Not all of the symptoms have an equal value for the lo- 
calization of a lesion. It is important first to note their mode 
of onset, whether this is sudden or gradual ; whether several 
symptoms have made their appearance at the same time or 
one after the other, and so on, for in acute lesions, for instance, 
only those symptoms which appear synchronously are of im- 
portance. If a patient who has a hemiplegia presents a paraly- 
sis of the oculo-motor of the opposite side, and we learn that 
this latter has existed before the onset of the hemiplegia, no- 
body certainly will think of connecting the two or look upon 
them as being symptoms due to one focal lesion. This would 
only be allowable if both had set in at the same time (after an 
acute lesion). 

But, even apart from the mode of onset, the symptoms are 
not of equal value in the localization. Some, it is true, as 
hemiplegia, together with contra-lateral oculo-motor paralysis, 
are almost pathognomonic (for a lesion in the cms), and their 
simultaneous appearance is therefore extremely important ; 
while others, as the conjugate deviation in severe hemiplegia, 
are found in different lesions, and are therefore less significant ; 
still others, as optic neuritis and all the general symptoms 
(headache, vertigo, unconsciousness), are absolutely valueless. 



x 66 DISEASES OF THE BRAIN PROPER. 

We see, therefore, that by no means all cases can be used 
for the study of the topical diagnosis, but that only those in 
which the affection, in the first place, remains chronically sta- 
tionary ; secondly, in which it is circumscribed and isolated 
(Nothnagel); and, thirdly, where the surroundings of the focus 
are as little as possible implicated. These three conditions are 
best fulfilled in instances of haemorrhage or embolus, or rather 
in the cases of softening produced by these accidents, and the 
largest contingent of cases which permit a topical diagnosis is 
therefore made up of these. They are rendered more suitable 
for our purpose the longer the time that has elapsed after the 
first onset (according to Nothnagel, six to eight weeks), as only 
then, as we stated above, are we able to separate the direct 
from the indirect symptoms. In other cerebral affections — e. g., 
meningitis, encephalitis, and especially tumors — a local diagno- 
sis should only be attempted with the greatest circumspection, 
and even then errors can not be altogether excluded. 

Symptoms Referable to Cortical Lesions. 

In speaking of cortical lesions, "surface lesions," it must 
not be forgotten that the clinical meaning of the term is differ- 
ent from the anatomical one. Anatomically, it implies that the 
medullary layer situated below the cortex is intact, while clin- 
ically we speak of cortical lesions even if the white matter 
takes part in the pathological process as well ; but so little at- 
tention has been paid to this difference in the autopsy reports, 
which have been published, that it seems an almost hopeless 
endeavor to distinguish whether the symptoms reported in a 
given case were due to changes in the cellular elements of the 
cortex itself, or to changes in the fibres of the medullary layer 
situated immediately beneath. 

We possess quite a considerable amount of material, but it 
is by no means easy to make a judicious and successful use of 
it. Certain methods have to be employed in order to arrive at 
correct conclusions, methods which have been developed in 
such an excellent way by Exner (cf. lit). It would, for exam- 
ple, be incorrect to assume a certain cortical area to be the 
centre for the motor function of an extremity simply because 
in many cases a lesion of this area was found where a paralysis 
in that extremity had existed during life. This " method of 
positive cases," as Exner has called it, is therefore uncertain, 
because there are quite different circumscribed cortical regions, 



CORTICAL LESIONS. !$- 

a lesion in which gives rise to the same symptoms ; and since, 
moreover, facts go to show that such a method may lead us to 
wrong conclusions, it ought to be discarded. Much more pref- 
erable, however, is the so-called " method of negative cases " 
(Exner), according to which " we have to mark out the lesions, 
found in all the cases in which a given function was not inter- 
fered with, and unite them on one hemisphere." If the number 
of cases is sufficiently large, while on the remaining parts of the 




Fig;. 38. — Right Hemisphere. (After Exner.) The portions shaded in represent those 
parts of the cortex which can be injured without giving rise to sensory or motor dis- 
turbances ; the blank areas are motor and sensory. 



cortex we find markings indicating lesions, the area for the 
functions in question will remain free. 

Still better results are obtained by the method of percent- 
ages (Exner). The cortex is divided into arbitrary fields, and 
for each of these fields we determine, first, how often it has 
been diseased in a given number of cases ; secondly, in how 
many of the cases the symptom which we are studying was 
present. The ratio between these two results is best given in 
percentages. Only through this indispensable, although some- 
what tedious, method can we ascertain that the fields of the 
right cortex are different from those of the left, and that cer- 



j 58 DISEASES OF THE BRAIN PROPER. 

tain areas exist of which a lesion always, and others of which a 
lesion not always but frequently, produces a certain symptom. 
The former Exner calls " absolute," the latter " relative," corti- 
cal areas. 

We do not always find cortical lesions at the autopsy in 
cases in which certain symptoms, which would have led us to 
suspect their existence, have been noted in life. On the other 
hand, they are found in cases where we have hardly felt justi- 
fied in expecting them. There is no doubt that no inconsider- 



Fig. 39.— Left Hemisphere. (After Exner.) This diagram illustrates that the motor 
and sensory areas are of a greater extent on the left than on the right hemisphere. 

able part of the cortex can be diseased without giving rise to 
any symptoms. It is this part which has been called the cor- 
tical area of latent lesions (Exner), and it is certainly a matter 
worthy of note that the extent of this area is smaller on the 
left than on the right hemisphere, whereas the motor area — 
that is, the area in which a lesion is followed by motor disturb- 
ances — is larger and more developed on the left than on the 
right side (cf. Figs. 38 and 39). The first represents the right, 
the second the left hemisphere. On both all the lesions are 
indicated which have produced neither sensory nor motor dis- 



THE BRAIN CORTEX. i6g 

turbances. The blank fields are therefore sensory and mo- 
tor — their greater extent on the left side is at once ap- 
parent. 

Before we go into the description of the individual lesions 
of the cortex we will briefly refresh our memory on the anat- 
omy of the parts. 

The thin gray covering which surrounds the white matter, and 
which has been called brain cortex, presents on each hemisphere 




Fig. 40.— Convolutions and Fissures of the Lateral Aspect of the Brain. 
(After Ecker.) Parallelfurche = parallel fissure, or first temporal fissure. 



three surfaces — a lateral, a basal, and a median. The two lateral 
form the convexity, the two basal the base of the cerebrum. The 
cerebrum is divided into lobes, which can again be subdivided into 
convolutions or gyri. To be able to localize and correctly describe 
cortical lesions we must be thoroughly familiar with the position, as 
well as the names, of the different convolutions. The following 
illustrations are intended to facilitate the study of the convolutions 
and the fissures or sulci separating them. Fig. 40 represents those 
on the lateral surface (convexity), Fig. 41 those on the basal, and 
Fig. 42 those on the median aspect of the cerebrum. 

In Fig. 40 are included the frontal, parietal, temporal, and oc- 
cipital lobes, so far as their convolutions and fissures belong to the 



7o 



DISEASES OE THE BRAIN PROPER. 



lateral surface, in other words, belonging to the frontal lobes, the 
three frontal and the anterior central convolution (gyrus centralis 
anterior, pit frontal ascendant), and belonging to the parietal lobe, 
the posterior central convolution (gyrus centralis posterior, or pit 
parietal ascendant) ; between the two last is seen the fissure of Ro- 
lando. Further, a part of the upper and the entire lower parietal 
lobe are shown, which latter is subdivided into the supra-marginal 
convolution in front and the angular gyrus (/// courbe) behind ; be- 
longing to the temporal lobe we have the three temporal convo- 
lutions, of which the first (uppermost) lies between the fissure of 
Sylvius and a very deep fissure running parallel to it, the so-called 




Fig. 41. — Convolutions and Fissures at the Base of the Brain (diagrammatically 
after Ecker). Hirnschenkel = crura cerebri. Balken = corpus callosum. 



parallel fissure or first temporal fissure. The fissure of Sylvius has 
two branches, and the portion of the cortex between them is called 
the " Operculum." Belonging to the occipital lobe, finally, there 
are three irregular and not always easily distinguishable occipital 



THE BRAIN CORTEX. 



171 



convolutions, between which two occipital fissures have been de- 
scribed. 

On the basal aspect we see those parts of the three frontal con- 
volutions which are included in the base, of which the first (upper- 
most) is here called the gyrus rectus; then the tractus, with the 
sulcus olfactorius; next the uncinate gyrus, which belongs to the 
gyrus fornicatus and which will be better seen on the median aspect ; 
further, the basal part of the third temporal convolution (gyrus tem- 
poralis inferior) and two lobules, which belong to both the temporal 




Fissura Mipjpoc. 



Fig. 42. 



Timbria res p. Tor nix. 

-Convolutions and Fissures of the Median Aspect of the Br^in. 
posterior portions of the thalamus and the crus cerebri are cut off. 



The 



and occipital lobe, the inner (median) one called the lingual lobule, 
the one more external the fusiform lobule. 

The median surface (Fig. 42) shows in the middle the corpus 
callosum (in front the genu, behind the splenium) ; immediately be- 
low is the "septum lucidum," immediately above the gyrus forni- 
catus, the temporal part of which is called the hippocampal convolu- 
tion, and is continuous with the uncinate gyrus. Above the gyrus 
fornicatus, and separated from it by the calloso-marginal fissure, are 
the frontal convolutions; further back, the paracentral lobule, which 
meets the central convolutions. Behind this and belonging to the 
parietal lobe is the precuneus, and still further back the cuneus (of 
the occipital lobe). The latter is bounded by two deep fissures — 
below by the calcarine, in front by the occipito-parietal fissure. 
Extending from the posterior part of the corpus callosum to the 
uncinate gyrus is the hippocampal fissure. 



172 



DISEASES OF THE BRAIN PROPER. 



Covered by the above-mentioned operculum, in the depth of the 
fissure of Sylvius, is the lobus intermedius s. opertus, the so-called 
island of Reil, on which five to seven small convolutions are seen. 




Fig. 43. — Convolutions of the Island of Reil (J. R.) made visible by removing 
the Operculum. 

Their position is shown in Fig. 43, where the operculum has been 
removed. 

In Fig. 44 the topographical relation between the surface of the 
brain and surface of the skull is illustrated. 



Among the parts which most frequently may be the seat of 
lesions without producing- any consequent sensory or motor 
disturbances during life is the frontal lobe. Some convolutions 
— viz., the first and second frontal — are certainly not to be 
reckoned as forming part of the motor area (cf. Figs. 38 and 39, 
with the lesions marked on the frontal lobe). On the other 
hand, of great significance and importance is the anterior cen- 
tral convolution, as a part of the so-called motor region, and 
the third (lowest) frontal convolution of the left hemisphere,. as 
the area of speech. To the motor region belong not only the 
anterior, but also the posterior central convolution, and the 
paracentral lobule. Extensive lesions of this region, foci of 
softening, which cause destruction of the cortex, produce symp- 
toms which collectively give us the picture of cerebral hemi- 
plegia, of which we shall give a more minute description later 



CORTICAL LESIONS. 173 

on. Circumscribed lesions produce affections of the individual 
centres of the extremities (absolute cortical areas, Exner), and 
give rise to symptoms either of a paralytic or of an irritative 
nature. To the latter belongs, among others, the so-called 
symptomatic or Jacksonian epilepsy. 

That the cortex of the frontal lobes is the seat of the higher 
psychical functions is shown by the changes which are found 
in certain forms of idiocy, often also in dementia paralytica, 
where wide-spread disease on both sides has been observed — 




Fig. 44. — Topographical Relations between the Exterior of the Skull and 
the Surface of the Brain. (After Ecker.) C, fissure of Rolando. V.C., ante- 
rior central, H. C, posterior central convolution. SS.S,, fissure of Sylvius. T, tem- 
poral lobe. F, frontal lobe. P t , upper, P n , lower parietal lobe. O, occipital lobe. Cb, 
cerebellum. 

viz., chronic inflammatory processes, atrophy of the convolu- 
tions of the right as well as of the left frontal lobe. 

The functions of the cortex of the parietal lobe are entirely 
obscure. Lesions in the upper parietal lobe have often been 
observed after paralysis in the extremities ; but in this connec- 
tion we should never lose sight of the influence of the posterior 
central convolution, which belongs to the motor region. The 
statement that it is in the lower parietal lobule, especially in its 
posterior part (angular gyrus), that the centre for the move- 
ments of the levator palpebrae superioris ought to be looked 



174 



DISEASES OF THE BRAIN PROPER. 



for (Landouzy) has as yet to be proved, and the relation which 
the parietal lobe bears to sensibility is equally obscure, not- 
withstanding the disturbances in muscular sense which have 
often been observed in diseases of this region (Bastian, cf. lit.). 

In the cortex of the temporal lobe, in the first temporal con- 
volution, most commonly on the left side, important centres of 
the auditory nerve are situated, and it is most probable that 
lesions of this region give rise to central deafness in the ear 
of the opposite side. Lesions of the first left temporal con- 
volution give rise to "sensory aphasia" (Wernicke), "word 
deafness" (Kussmaul). Motor disturbances have never been 
found associated with diseases of the temporal convolutions. 

The cortex of the occipital lobe finally contains the centre 
for the opticus, and lesions of sufficient extent in this region 
produce hemianopia (cf. page 34). Quite a number of post- 
mortem examinations seem to point to the first occipital con- 
volution and to the cuneus as the seat of the centre for vision. 
The interesting fact, observed by Fiirstner, that certain pa- 
tients, although able to see objects before their eyes, are unable 
to recognize them — i. e., have forgotten their significance — is 
also a consequence of lesions in the occipital cortex ; the mem- 
ory for optical pictures is lost, and we have what is called a 
psychical blindness (Munk). Motor disturbances (paralysis, 
spasms) are not caused by diseases of the occipital convolu- 
tions. 

The convolutions of the island of Reil are but rarely af- 
fected by themselves, usually other parts, the third frontal 
convolution, the centrum ovale, etc., being also implicated ; it 
is therefore impossible at present to state with any certainty at 
all in what way speech is connected with the insula of the left 
side, and to give the relations between pathological conditions 
in this part and aphasic symptoms. 

While from what has been said we see that the functions of 
a large part of the cerebral cortex are as yet obscure — in other 
words, that the " area of latent lesions " is of lamentably large 
dimensions — we have, on the other hand, the satisfaction of 
knowing that the significance of some areas is understood with 
a fair amount of clearness. It is true even these can to a large 
extent only be regarded as " relative " (in the sense of Exner), 
for, as we shall presently see, there are only very few "abso- 
lute " areas. 



APHASIA. 



175 



In the motor region of the right side, the paracentral lobule, 
the anterior central convolution, and the upper part of the 
posterior central convolution, on the left side, the paracentral 
lobule, the three upper quarters of the two central convolu- 
tions, and a part of the upper parietal lobule, are properly 
called the absolute cortical area for the upper extremity (Ex- 
ner). The absolute area for the lower extremity is formed by 
the paracentral lobule and the upper third of both central 
convolutions on the right side, on the left by the paracentral 
lobule, the upper half of the posterior central convolution, and 
the greater part of the upper parietal lobe. 

The cortical area of the trigeminus has been spoken of on 
page 55, that of the facial on page 78, and that of the hypo- 
glossus on page 142. Of the centres for the eye muscles, espe- 
cially for the levator palpebral, mention has been made in the 
third chapter of the second part (cerebral blepharoptosis, page 

44)- 

The speech centre, which, as we have seen, is situated part- 
ly in the frontal, partly in the temporal lobe of the left hemi- 
sphere, is certainly of larger extent than is commonly sup- 
posed. It is well known that after Bouillaud in 1825 had 
pronounced the frontal brain, and Marc Dax in 1836 the left 
hemisphere, to be the seat of speech, Broca claimed that the 
posterior part of the third left frontal convolution, the pars oper- 
cularis, or, as it later was called, the region of Broca, contained 
the speech centre ; and, indeed, in speech disturbances a lesion 
of this very region has most frequently been found at the au- 
topsy. There are, however, other parts of the cortex, as the 
island of Reil, the central convolutions, and, above all, the tem- 
poral lobe, more especially its upper convolution, which are 
connected with speech and which are of no less importance. 
Thus we have, after much laborious work and after many care- 
ful observations and comparisons, come to the conclusion that 
a different form of speech disturbance (aphasia) is produced 
according as the lesion is one of the frontal or of the parietal 
lobe — (of the left side only). In the former case the patient 
knows the word which he wishes to pronounce, but can not do 
so because he has lost the memory for the movements neces- 
sary for speech — i. e., he no longer knows how to use his 
tongue and lips in the act of speaking — motor aphasia. In the 
latter case the patient knows exactly what he wants to say, 
and he has no difficulty in repeating it if it is spoken for him ; 




iy6 DISEASES OF THE BRAIN PROPER. 

but he can not find the expression for himself, he has " forgot- 
ten " the word — sensory aphasia. That the understanding- of 
words is situated in the temporal lobe was first stated by 
Wernicke, who also originated the terms motor and sensory 
aphasia. 

In the diagram of Wernicke which is shown in Fig. 45, y 
represents the motor, x the sensory speech centre ; the latter 

is the terminus of the 
centripetal path of the 
auditory nerve a x, the 
former is the beginning 
of the centrifugal path 
y m going to the mus- 
cles used in speaking ; 
x y an assumed associa- 
tion path between both ; 
y is situated in the third 
frontal, x in the first 
45-Wernicke's Schema for the Cortical temporal convolution. 
Mechanism of Speech. r 

According as one or 
the other of these centres or the connection between them, or 
both centres were destroyed, Wernicke distinguished four 
cardinal types of aphasia : 

1. Destruction of the centre y — motor aphasia. Mobility 
of the muscles used in speech is retained, but the patient can 
either not speak at all or only say a few words or syllables. 
Understanding and memory of words is intact. 

2. Destruction of the centre x — sensory aphasia, " word deaf- 
ness " (Kussmaul). The patient can use as many words as ever, 
but in speaking they are mixed up. The understanding of words 
is lost, although the power of hearing is not interfered with. 

3. Destruction of the association path x y, situated in the 
insula (?) — the so-called conduction aphasia of Wernicke. The 
patient can use as many words as ever, but in speaking they 
are mixed up. The understanding of words is retained. 

4. Destruction of both centres, x and y — total aphasia. 
Power and understanding of speech are lost. 

If we then consider as proved that a certain group of motor 
and sensory memory pictures are localized in the brain, if we 
further agree that the former correspond to certain groups of 
muscles which serve a common purpose, the latter to the dis- 
tribution of a sensory nerve — it is not difficult to conceive that 



APHASIA. 



1 77 



this same arrangement may exist for all the muscles and for 
all the sensory nerves. It is certainly easy to understand the 
occurrence of other motor defects in cases of aphasia. Thus 
there may be loss of simple movements (e. g., of the power to 
put out the tongue), or more complex ones (e. g., writing may 
become impossible — agraphia ; aphasie de la main, Charcot). 
Again, we have a patient who, in consequence of a cortical 
lesion in the central termination of the optic nerve, no longer 
recognizes his letters, and has thus lost the faculty of reading 
("alexia"), or the visual memories may be lost altogether (not 
only those of letters), and a condition ensue which Munk calls 
psychical blindness. 

In examining a patient affected with aphasia, with a view 
of determining which path has become interfered with, we may 
meet with considerable difficulty, and the diagnosis of the par- 
ticular type of aphasia with which we are dealing is often not 
easy, for the cases are not so sharply defined or so well charac- 
terized as we might be led to expect from the simplicity of 
the schemata. On the contrary, we meet often with combina- 
tions of the different types or with transition forms of aphasia 
in which even the most experienced clinician will venture a 
differential diagnosis only with much reservation. Take, for 
instance, the different degrees of that form of speech disturb- 
ance known as ataxic aphasia, in which the patient is unable to 
pronounce a word, though it constantly is floating, as it were, 
before his mind. This inability may go so far that the patient 
can only pronounce a few words or syllables (monophasia), 
that he involuntarily confounds words without being in the least 
uncertain about their meaning; or it may, on the other hand, 
only amount to a slight disturbance, shown by some misplace- 
ment or omission of some letters, as in saying dy instead of 
dry, tnrk instead of truck, and the like. In the latter case we 
speak of syllable-stumbling (Silbenstolperti). Likewise we have 
different degrees of the so-called amnesic aphasia, where there 
may be loss or only slight impairment in the memory for words 
(sometimes only for words of foreign languages which have 
been learned later in life). As the faculty of writing and read- 
ing may often be more or less altered, it is important that it 
should be minutely examined into. Every case of aphasia must 
be carefully studied by itself, and in each one is bound to find 
some interesting points which we can not now stay to discuss 
in detail. 



!^8 DISEASES OF THE BRAIN PROPER. 

In general we may be guided by the following rules : 
i. If we find a patient whose sanity is established, who pos- 
sesses a normal acuteness of hearing and understands what is 
said, but is unable to repeat sentences or to speak spontaneous- 
ly, and can only utter individual words and syllables, we may 
assume a lesion of the third frontal convolution, possibly of the 
lowest part of the anterior central convolution. 

2. If a patient, although able to speak without difficulty, 
does not understand simple questions, then the first temporal 
convolution is diseased {in totd). If the understanding of words 
is only impaired, then only a part is affected. 

3. If the patient has lost the faculty of reading, although 
there is no motor aphasia to be noted, we have to deal with a 
lesion of the cortical centre for vision (cf. page 29). 

4. A disease of the cortical speech centre does not exist if 
the patient gradually regains speech which he had suddenly 
lost ; if in such a case the hemiplegia, which has simultaneously 
appeared after an apoplectic stroke, persists, the white sub- 
stance near the cortex is wont to be diseased (Gowers). 

We should be going beyond the limits of our work if we 
examined into all the details of the complex symptomatology 
of aphasia, difficult, and indeed in some phases still uncertain, 
as it is, the more so as there exist quite a large number of ex- 
cellent special works dealing with this subject, an acquaintance 
with which is indispensable for the more accurate study of 
these interesting affections. Let it suffice to outline the differ- 
ent forms of aphasia, and this, according to our experience, will 
be best and most easily accomplished with the aid of schemata, 
of which", besides the above-mentioned one of Wernicke, quite 
a number have been brought out. The one we have deemed 
most suitable and the best fitted for teaching purposes is prob- 
ably that which Lichtheim demonstrated at the conference of 
neurologists at Baden Baden in 1884. It has been here given 
in Figs. 46 and 47. 

The reflex arc necessary for repeating words contains the 
centre for auditory images of words, A, the centre for motor 
images, M, the centripetal path for auditory impressions, a A, 
the connecting path, A M, the centrifugal motor path, Mm. B 
is the place where concepts are formed — voluntary speech 
necessitates a centrifugal path from B (brain cortex) to M. O 
is the centre for the visual images of letters. E is the centre 
for the innervation of the muscles required in writing. Now, 



APHASIA. 



179 



according to the path affected, we distinguish seven different 
forms of aphasia : 

1. Interruption in the point M. 



2. Interruption in 
point A. Wernicke's 
(sensory) aphasia. 

3. Interruption in 
the path M A. Con- 
duction-aphasia (Wer- 
nicke). 

4. Interruption in 
the path MB. A va- 
riety of motor apha- 
sia ; the faculty of re- 
peating words and 
sentences being re- 
tained. 

5. Interruption in 
the path M m. Va- 
riety of motor aphasia ; 
the power of express- 
ing thoughts in writ- 
ing being retained. 

6. Interruption in 
the path A B. A va- 
riety of sensory apha- 
sia ; the patient being, 
however, able to re- 
peat spoken language, 
to read aloud, and 
write from dictation. 

7. Interruption in 
the path A a. Inabil- 
ity to understand spo- 
ken language and to 
write from dictation, 
or to repeat spoken 
language. Numbers 
six and seven have not 
yet been observed. 

As to the occur- 
rence of aphasia, it 



Broca's (motor) aphasia. 
B SB 




Fig. 46. 




Fig. 47- 
Figs. 46, 47. — Lichtheim's Schema illustrating the 
Seven Different Forms of Aphasia, a. A., cen- 
tripetal path for auditory impressions. A, centre for 
auditory images. M, centre for motor images. M, m, 
centrifugal motor path. B, the place where concepts 
are formed. 0, the centre for visual images. E, cen- 
tre from which the organs of writing are innervated. 
(The seven different forms of aphasia have been in- 
dicated in Fig. 46 by the numbers 1-7.) 

is most frequently seen as a sequence 



j8o diseases of the brain proper, 

to an apoplectic attack, either as a direct or indirect 
symptom ; in the latter case it is transient, and lasts, as 
we shall see later, a few minutes, hours, or days. In the 
former it persists, and may trouble the patient, though he may 
retain his full mental vigor, to the end of his life. The most 
common form is motor aphasia, which appears in widely dif- 
ferent gradations ; thus, in some cases the patient's speech 
may be just a little thick, while in others it may be altered so 
that it is no longer intelligible. After what has been said, it 
is easy to understand that these defects chiefly occur after 
haemorrhage in the left side of the brain — that is, with a right- 
sided hemiplegia — but it would be a decided error to suppose 
that they occur only or always in those cases, for motor apha- 
sia may indeed be found in connection with a left-sided hemi- 
plegia, and it may be wanting in the right-sided form. Other 
diseases also may implicate the cortical speech centre and give 
rise to aphasia ; such are processes of softening, chronic men- 
ingitis, tuberculous deposits, etc., and traumatism of the left 
hemisphere. Aphasia has also been observed in acute, espe- 
cially infectious, diseases — e. g., typhoid and scarlet fever. 
Most instances of this latter form occur in children. Of 
special interest is that form of total or motor aphasia which 
sometimes suddenly, sometimes gradually, comes on after a 
fright. That after a fright, such as makes " the hair stand on 
end," the voice may refuse to perform its duty even Virgil 
seems to have known full well, as we see from the verse, " Stet- 
erantqiie comes, vox fancibus hcesit." The nature of this form is 
uncertain, still it is by no means impossible that, just as we find 
that vaso-motor spasm acting on the facial vessels will pro- 
duce pal^Dr, so we may have a similar condition in those finest 
distributions of the middle cerebral artery which supply the 
region of Broca (cf. page 175). That the spasm in these ves- 
sels is usually of longer duration and produces more serious 
and more lasting consequences than the spasm of the cutaneous 
vessels may be explained by the difference in their arrangement, 
as well as by the difference in the function of the parts which 
they supply. 

It is not organic changes of the cortex which produce the 
symptoms in this case, the disturbances being entirely of a 
functional character, and this fright aphasia therefore consti- 
tutes a transition form to those instances in which, though the 
aphasia may have lasted for years, no changes are found at the 



APHASIA OF CHILDREN. jgi 

autopsy, either in the cortical or subcortical area for speech. 
No doubt there is, besides the aphasia due to actual lesions in 
the cortex, also a functional form which we may imagine to 
originate in different ways, and it is at least probable that 
variations in the blood supply of the centres play an important 
part in this connection. Not long ago Grashey (cf. lit.) has 
shown, in an ingenious piece of work, that we have to recognize 
a third form of aphasia, in which neither the centres nor the 
conducting paths are insufficient in their functions, but which 
is simply due to a diminished duration of the sensory impres- 
sions, giving rise to a disturbance in perception and associa- 
tion, and thus to an aphasic condition. Maybe it is this apha- 
sia of Grashey which we find after concussion of the brain 
and after acute diseases, but it is difficult to diagnosticate it, 
and to differentiate a functional disturbance of the centres 
from a diminished duration of sensoiy impressions. A correct 
diagnosis is, however, of no small importance in the question 
of prognosis. 

The outlook is absolutely unfavorable in cortical lesions 
where the centre is destroyed by processes of softening, tuber- 
culous deposits, atrophy of the gray cortex, etc., but is, of 
course, materially better if the centres remain intact, and are 
only temporarily rendered unable to perform their function, 
for then speech returns gradually, if not wholly, partially, and 
it can not be denied that systematic exercise and regular in- 
struction in speaking is capable of hastening an amelioration, 
nay, even a cure, especially if the patient be still young. 

The by no means rare aphasia of children, which we some- 
times find in consequence of intestinal worms (" reflex aphasia "), 
in the course of acute infantile cerebral palsy, occasionally, but 
very rarely also, after a cerebral haemorrhage, is in no other 
way to be distinguished from the aphasia of adults except in 
its prognosis. Children, ceteris paribus, always stand a better 
chance of improvement or recovery from aphasia than adults, 
no doubt because it is easier to educate in them the well half 
of the brain to perform the function of the damaged one. If 
the disturbance is only functional, as I saw in one case which 
was due to an overdose of santonin, in which the disorder in 
speech only lasted a few hours, the outlook is still more favor- 
able, and complete recovery may be confidently expected ; but 
if the function of one speech tract — that is, the left — be im- 
paired by cortical or deep-seated lesions, even then it is in 



lS2 DISEASES OF THE BRAIN PROPER. 

children usually not very difficult to educate the right side to 
some vicarious action, especially in cases where, before the 
lesion, the children have been taught to use both hands equally. 
The possibility of a cerebral disease should be thought of in 
the gymnastic cultivation and development of the body of 
children ; the extremities of both sides should be exercised and 
strengthened equally, the children should be made ambidex- 
trous ; only then can, in a case of necessity, the right hemi- 
sphere fully take the place of the left. 

We have repeatedly pointed out that the motor disturb- 
ances produced by cerebral diseases are either due to destruc- 
tive or irritative lesions. The former consist of paralyses and 
pareses, the latter of involuntary movements in different groups 
of muscles — the so-called spasms. Those disturbances which 
are due to affections of the cortex (cortical motor disturbances) 
present much that is characteristic and interesting. They will 
be considered presently. 

The motor centres, the motor area of the cortex, comprise, 
as has already been stated on page 172, the two central con- 
volutions, the paracentral lobule and the parts lying imme- 
diately adjacent. Upper and lower extremities, neck and face, 
have their own special centres, which are distinctly separated 
from one another in the central convolutions. Thence fibres 
converge, as is shown in the diagram of Fig. 48, into the ante- 
rior two thirds of the posterior division of the internal capsule. 
One thing at once becomes apparent from this arrangement, 
namely, that in cortical lesions the paralysis or paresis may 
easily be confined to one extremity, an arm or a leg, while if 
the lesion affects the tract lower down in the brain — for in- 
stance, in the region of the capsule — the paralysis must extend 
over the whole half of the body. A paralysis of one extremity 
only is called a monoplegia (monoparesis) in contradistinction 
to a hemiplegia, which means paralysis of one side (half) of the 
body, and it is a perfectly warrantable conclusion, sufficiently 
confirmed by post-mortem evidence, that, if the patient pre- 
sents a paralysis of only one arm or one leg, we are dealing 
with a cortical lesion. A hemiplegia is only then likely to be 
of cortical origin if its development indicates that the lesion 
beginning in one motor centre has gradually encroached upon 
another. It goes without saying that in diagnosticating cor- 
tical lesions we must not rely on a single symptom, but all 
must be considered, and especial care must be taken not to 




CORTICAL MOTOR PARALYSIS, ^3 

confound a paralysis of cortical with one of peripheral origin. 
One great distinction between these two is to be found in the 
manner of onset. While a paralysis of cortical origin may de- 
velop quickly in a few hours, a peripheral one will be more 
gradual, and only reach its full extent after weeks or even 

7 7 

i / 
>N / / / .^ 

zfcfj/s ^jp***- 

Lenticular nucleus h "">;'^<?"~ ■•'' ' ?7::: ^ — ~ — _ 

\ \" 

«—.— . i^ Pyramidal tract. i\' V. ~*./i*rp-JL Nucleus dentatus 

» V\ ''V'' ^TS^ cerebelli 

• ■ ■ Frontal cortico-pontine • #\x •- .^^V"^ 

fasciculi. 1^ LX^° 

. Temporo-occipital corti- » v ?s\.^^^^^^C a 

co-pontine fasciculi. tf^.^** 

Ant. and post, cerebello- » *\ 

pontine fasciculi. • » 

Tegmental radiation and » I 

sup. peduncle of cere- • \ 
bellum. \ 

Ansa lenticularis. » \ 

\ 9 Crossed pyramidal tract 

x — x_— x— x_— x. Cortical fillet (psycho- 1 

sensory paths). ^ Uncrossed pyramidal tract 

I 
Fig, 4 8.— Diagram showing the Direct System of Fibres (Flechsig, Mendel). 

months. Moreover, the latter, the peripheral, is easily recog- 
nizable by the changes which take place in the electrical excita- 
bility — e. g., if reaction of degeneration and visible atrophy in 
the muscles can be demonstrated. The absence of cerebral 
symptoms, which are rarely entirely wanting in cortical affec- 
tions, is also characteristic of peripheral disease. Great pain 
may be entirely absent in the central, but is commonly present 
to a greater or lesser degree in the peripheral variety. Re- 





!84 diseases of the brain proper. 

membering then these points, and making it a routine practice 
never to omit the electrical examination in doubtful cases, we 
are not likely to make an error in the diagnosis. 

In cortical lesions the loss of motion is usually not absolute, 
and we find more frequently a paresis than an actual paralysis. 
The affected arm or leg can be moved in toto, though a strong 
effort may be required, and it is only in the fingers and toes 
that the loss of power is often complete. 

A characteristic symptom is the inability of the patient to 
execute complicated movements, such as buttoning his coat, 
counting money, and so forth, acts which are performed awk- 
wardly and with difficulty, owing to a loss of the motor im- 
ages. This condition has been called ataxia, and in these cases 
we have a " cortical ataxia." The lesion has to be referred to 
that part of the cortex which contains the sensory area {Fiihl- 
sphare of Munk) for the affected, that is, the ataxic extremity. 
The trouble is very distressing to a patient in a brachial as 
well as in a crural monoplegia, and becomes almost unbearable 
if the sensory disturbances, which we shall shortly describe, are 
superadded (cf. lit., Observations of Bernhardt). 

In infective tumors, gummata, tubercles at the surface of 
the brain, we occasionally meet with symptoms of irritation, 
such as monocontractures, which depend upon an irritation in 
the corresponding portion of the motor path (Wernicke). 
They are not seldom accompanied by sharp pains. In such 
cases the differential diagnosis between a hysterical and a true 
organic cortical lesion may cause considerable difficulty (cf. 
chapter on hysteria). 

Of the greatest practical importance are the epileptiform 
attacks which occur, either with or without loss of conscious- 
ness, as a consequence of direct or indirect irritation of the 
cortex. If they occur in the further course of the monoplegia, 
the onset of which was apoplectiform, the diagnosis of a corti- 
cal lesion can be made with a high degree of probability. In 
some cases the convulsions are not general, but only appear as 
localized twitchings or spasms, confined to one half of the body 
or one extremity ; they may be clonic (that is, an alternation in 
quick succession of contractions and relaxations) or tonic (that 
is, steady contractions lasting for some time), and may be of 
considerable intensity ; their occurrence later in parts already 
paralyzed would indicate a disease of the brain surface, though 
we may not always be able to say whether the irritation of the 



CORTICAL SENSORY CHANGES. 



■85 



cortex depends upon a direct or — as, for instance, in tumors, 
which cause an increase of the intracranial pressure — an indi- 
rect action. In the latter cas:, also, general or partial convul- 
sions may ensue. 

We shall later on have occasion to go more thoroughly 
into the study of the clinical picture as well as the pathologi- 
cal changes of this " cortical epilepsy." 

The sensory disturbances which are produced by the affec- 
tions of the brain cortex are remarkable, and by no means fully 
understood. As we have seen before, they do not, as a rule, 
cause pain, but rather manifest themselves in alterations of 
sensation, known as paresthesias. Thus the patient may speak 
of a curious numbness, deadness — further, a feeling of ants 
crawling under the skin, a feeling as if the part had gone to 
sleep, etc. There may also be a distinct increase in pain per- 
ception, a slight " analgesia," a diminution or loss of pressure, 
touch, and temperature sense, and, oftener as it seems in dis- 
eases of the parietal lobes, a more or less pronounced disturb- 
ance of the muscular sense, in consequence of which the pa- 
tient can with closed eyes either give no account at all or only 
a very imperfect one of the position of his extremities. If, as 
often happens, the above-described awkwardness in motion 
(ataxia) co-exists with these changes, we may be tempted to refer 
the trouble not to the cortex, but to the spinal cord ; more espe- 
cially are we liable to think of tabes, although the ataxia is 
produced in an entirely different manner in the two diseases. 
However, the differential diagnosis will in most cases present 
no difficulties if we take into consideration all the symptoms, 
and examine into the condition of the patellar reflexes, the re- 
action of the pupils, and ascertain whether there are bladder 
symptoms and whether lancinating pains are present or not. 
These sensory changes, which we must not forget, are by no 
means always observed in cortical lesions, and in the cases 
in which they existed the white matter of the brain has often 
been found to be likewise the seat of disease ; they are there- 
fore in no way to be regarded as pathognomonic, and we have 
to be cautious in using them for diagnosis. The same is true 
to a greater degree of the vaso-motor and trophic changes, the 
relation of which to the brain cortex is still obscure. 



!86 DISEASES OF THE BRAIN PROPER. 

LITERATURE. 

A. Physiology. 

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hirn. v. Volkmann's Sammlung klin. Vortr., 113. Leipzig, 1877. 

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Munk. Zur Physiologie der Grosshirnrinde. Gesammelte Mittheil. aus den 
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Goltz. Ueber die Verrichtungen des Grosshirns. Bonn, 1881. 

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B. Pathology. 

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(Cf. lit. in chapter on epilepsy.) 

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Heilk., ii, 5, 1881. 
Wernicke, loc. cit., i, pp. 199, 324 et seq., 1881. 
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arztl. Zeitschr., 22, 1884. 
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Nervenheilk., vii, 1, 1884. 



LITER A TURE. 



187 



Berger. Zur Localisation der corticalen Sehsphare beim Menschen. Bresl. 

arztl. Zeitschr., 1, 3-5, 1885. 
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scher-Vers., in Strassburg, 1885. 
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Annalen, xi, p. 538, 1886. 
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Clowes & Sons, 1886. 
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corticalen Sehstorungen. Arch. f. Psych, und Nervenkrankh., xviii, 3, 1886, 

& xix, 1887. 
Joffroy. Arch, de physiol., 15 fevr. 1887. (Monoplegia of the lower extremi- 
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Wochenschrift, 47, 1887. 
Bouveret. Lyon med., lvi, p. 337, 1887. 
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Centralbl. f. Nervenheilk., x, 1, 2, 1887. 
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vista clin. Settembre, 1887. 
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Med. Sc, Jan., 1887. 
Poore. Clin. Soc. Transactions, xx, p. 226, 1887. 
Nothnagel. Ueber die Diagnostik der Gehirnkrankheiten. Deutsche med. 

Wochenschrift, xiii, 15, 16, 1887. 
Senger. Ueber topische Him diagnostik und Hirnchirurgie, etc. Deutsche med. 

Wochenschrift, xiii, 10, 13, 1887. 
Siemerling. Deutsche med. Zeitung, viii, 25, 1887. 
Chauffard. De la cecite subite par lesions combinees des deux lobes occipitales 

Revue de med., 2, 1888. 
Welt, Leonore. Ueber Charakterveranderungen des Menschen in Folge von 

Lasionen des Stirnhirns. Deutsch. Arch. f. klin. Med. Bd. 42, Heft 4. 

(Diminution of intelligence, deterioration of the character.) 

2. The Speech Centre (Aphasia). 

Wernicke. Der aphasische Symptomencomplex. Breslau, 1874. 
Wernicke. Lehrbuch der Gehirnkrankheiten, loc. cit., v, p. 366 et seq., 1881. 
Charcot. Des varietes de 1'aphasie. Progr. med., 23-27, 1883. 
Lichtheim. Arch. f. Psych, und Nervenkrankheiten, xv, 3, 1884. 
Lichtheim. On Aphasia. Brain, January, 1885. 

Kussmaul. Die Storungen der Sprache. 3. Auflage, Leipzig, 1885. Cf. Ziems- 
sen's Cyclopaedia of the Practice of Medicine. Wood & Co., New York, 1887. 



Z 88 DISEASES OF THE BRAIN PROPER. 

Wernicke. Die neueren Arbeiten iiber Aphasie. Fortschritte d. Med., iii, 24, 

1885. 
Grashey. Ueber Aphasie und ihre Beziehungen zur Wahrnehmungen. Arch, 

f. Psych, und Nervenkrankheiten, xvi, 3, 1885. 
v. Gudden. Ueber das Sprachcentrum. Miinchn. med.. Wochenschr., xxxiii. 

4, 1886. 
Coen, N. Zur Pathologie und Therapie der Sprachanomalien. Wien, 1886. 
Kauders. Wiener med. Jahrbuch, N. F., i, 6, p. 251, 1886. (Loss of the left 

speech centre, vicarious activity of the right hemisphere.) 
Ross, James. On Aphasia. London, 1887. 
Sigaud. Note sur un cas d'amnesie verbale avec autopsie. Prog, med., xv, 36, 

1887. 
Berlin. Eine besondere Art von Wortblindheit (" dyslexia"). Wiesbaden, 1887. 
Ferrand. L'exercise du language et l'aphasie. Gaz. des hop., 28, 31, 1887. 
Heinzelmann. Munch, med. Wochenschr., xxxiv, 12, 1887. 
Knecht. Deutsch. med. Wochenschr., 37, 1887. 
Brims. Ein Fall von Dyslexie mit Storungen der Schrift. Neurol. Centralbl., 2, 

1888. 
Charcot. De l'aphasie en general et de l'agraphie en particulier. Prog, med., 

5 fevr. 1888. 



Symptoms Referable to Lesions of the White Matter of the 
Hemispheres and Lesions of the Basal Ganglia. 

Looking at the anatomy of the parts, we notice that the fibres 
coming from the cortex pass through the white matter of the hemi- 
sphere, which in the region of the frontal and parietal lobes is 
designated centrum semiovale Vieussenii. Turning toward the brain- 
stem, in its neighborhood they appear arranged in bundles placed 
side by side, completing by their convergence what has long been 
known as the corona radiata. With this corona radiata begins the 
great nerve tract which connects the hemispheres with all parts of 
the brain situated lower down, and finally with the spinal cord. That 
part of the medullary path through which the corona radiata is con- 
tinued into the crura cerebri is called the internal capsule. As is 
seen in Fig. 49, this is situated anteriorly between the caudate and 
the lenticular nucleus, posteriorly between the lenticular nucleus 
and the optic thalamus. The point where the two segments meet 
is called the genu, the knee of the capsule. 

From the internal capsule the fibres reach the crusta (pes pedun- 
culi cerebri), whence they pass through the lower (anterior or ven- 
tral) portion of the pons and enter the medulla oblongata as the 
anterior pyramids. At the lower end of the medulla most of them 
decussate and pursue a downward course in the lateral columns of 
the spinal cord on the opposite side. This, the most important of 
all direct systems of fibres, was discovered by Deiters in 1865, and 



THE INTERNAL CATSULE. jgg 

most carefully studied by Flechsig in 1876. It is generally known 
as the lateral pyramidal tract, and it represents the path for the 
voluntary movements. A lesion of it is therefore of grave conse- 
quence for the motor functions. 

In Fig. 50 the position of the centrum semiovale is represented, 
while Fig. 51 gives another horizontal section in a plane somewhat 



mt Frontal lobe 



Anterior limb 

of internal 

capsule 

Nucl. caudat. 



Nuel. 
lentif. 



Posterior limb 

of internal 

eapsuh 




Fig. 49. — Course of the Fibres from the Internal Capsule to the Crus Cerebri. 
The thalamus is represented as transparent. (Diagrammatic after Wernicke and 
Edinger.) 



lower down, and shows the relative position of the caudate nucleus 
to the optic thalamus, the corpus callosum, the fornix, the two white 
commissures, the anterior and the posterior, the gray middle com- 
missure, the pineal gland, and the corpora quadrigemina. 

Fig. 52 is a third horizontal section through the cerebrum at a 
still lower plane. It has to be studied in conjunction with the dia- 
gram given in Fig. 48. 

Fig. 53 represents the base of the brain, with the superficial 
origin of the twelve pairs of cranial nerves (cf. Fig. 28). 

Figs. 54, 55, and 56 are three so-called frontal sections, of which 
the first is made through the anterior commissure, the second in 



I O0 DISEASES OF THE BRAIN PROPER. 

front of, the third behind the middle (gray) commissure. They also 
show the course of the internal and external capsule, and the situa- 
tion of the so-called basal ganglia, the caudate and the lenticular 
nucleus (together known as the corpus striatum), and the optic 
thalamus. 

In another frontal section, Fig. 57 (after Edinger), the direction 
of the fibres is illustrated diagrammatically. 

Pitres has recommended a series of frontal sections in order to 
facilitate in our descriptions of autopsies a more accurate localiza- 



Striae longitud. 



— Corpus caUosum 




Fig. 50.— Horizontal Section through the Hemispheres. 



tion of lesions and tumors within the very extensive white matter 
of the brain. Nothnagel has modified somewhat these sections of 
Pitres with regard to their position and designation. The table on 
page 196 contains the necessary explanation. With the help of these 
sections we need not content ourselves any longer with locating in 
the post-mortem accounts a tumor " in the anterior part of the 
brain," " in the temporal lobe," etc., but we give the one or more 
sections which correspond to the situation of the neoplasm, and so 



LESIONS OF THE CENTRUM OVALE. 



I 9 I 



attain an accuracy which is indispensable for the after-use of our 
autopsy records. 

Figs. 59 to 64 represent diagrammatically Pitres's sections. From 
Fig. 58 we can get an idea of the points on the surface of the brain 




Corp. callos. 

Ventric. later. 
Ventric. sept, pelluc. 
~Micl. caud. 
Fornix. 

■Commiss. anter. 
Commiss. media 
Tarda semicircularis 
Thalamus 
Commiss. poster. 

' Pineal gland 
JBulvinar 

Corpora, 
quadrigemina 



Fig. 51.— View of the Ventricles on Horizontal Section. (After Edinger.) 



at which the sections are to be made (cf. Pitres, Recherches sur les 
lesions du centre ovale des hemispheres cerebraux etudies au point de 
vue des localisations cerebrales, Paris, 1877). 

We can likewise avail ourselves of the charts of the human brain 
published by Exner (two plates, with twelve diagrams : Wien, Brau- 
miiller, 1888). On the plates the discovered lesion can be easily 
marked off, and thus the extent and situation of it represented. 

With reference to the lesions in the centrum ovale, it should 
be stated that, as a rule, the symptoms produced by them are 



192 



DISEASES OF THE BRAIN PROPER. 



similar to those which we find in lesions of the corresponding- 
area of the cortex. Thus we shall meet with motor disturb- 
ances if the fronto-parietal fasciculi of the corona radiata, which 
take their origin in the motor area, are diseased ; while lesions 
in the prsefrontal or occipital bundles may, and indeed very 
often do not evoke any symptoms. If the left (inferior) pedic- 
ulo-frontal bundles in addition are affected, the patient will 
also be aphasic, the aphasia, however, being of long duration 




Fig. 52.— Horizontal Section through the Brain, about a Finger's Breadth 

BELOW THAT REPRESENTED IN FlG. 51. (EDINGER.) 



only if the lesion extends close up to the cortex. Lesions in 
the white matter of the occipital lobe may produce hemianopia, 
in the temporal lobe auditory disturbances. Whether, how- 
ever, diseases in the parietal lobes ever produce sensory 
changes — anaesthesia, for instance — and whether, as a conse- 
quence of any lesion in the centrum ovale, vaso-motor-trophic 
changes may be developed, is unknown. 

The idea that the basal ganglia were true motor centres, 
and that the common form of hemiplegia was due to lesions 



THE BASAL GANGLIA. 



193 




Fig- S3-— Base of thk Brain (with the First Portion of the Spinal Cord). I-XIJ, 
the twelve cranial nerves, ncl, first cervical nerve. 



thereof, has been given up, and we have learned from the in- 
vestigations of Flechsig and Wernicke that direct connections 
between the motor centres of the cortex and these basal ganglia 
do not exist. Moreover, it has been proved by numerous thor- 
oughly reliable observations that destruction of the lenticular 
13 



i 9 4 



DISEASES OF THE BRAIN PROPER. 



or of the caudate nucleus does not necessarily give rise to a 
motor paralysis. One or both lenticular nuclei have repeatedly 




Corpus callosun. 

jSept jpeTluc. 

Jfucl. caudat. 

Caps. int. 

JSucl. lentif. 

Glaustrum 



Fig. 54- 

been found destroyed in cases in which there was no sign of 
paralysis (Lepine, Nothnagel). In order that this may not 



Uuel. caud. 



Corpus callosum- 
Crura forn 
Tlialam. 
Insula 
Caps. int. 
ISitel. lentiform 
Caps. ext. 
Claustr. 




Fig. 55- 

ensue, it is only necessary that the internal and perhaps also 
the outer capsule remain intact. As soon as the former (the 



LESIONS OF THE OPTIC THALAMUS. 



195 



^Sucl. caudi. 

IFornlx 
Thalamus 



Commissura molh 
[media) 
Nucl. tegment. 
(red nucleus) 
Subst. nip:- — H: 
Pes pedunculi 



Gyr. Jlijopoe.^ 

Fig. 56. 

There is no doubt but 
cially of its anterior and 
middle part, may occur 
without symptoms, and 
it is impossible to say 
whether motor paralysis 
is ever produced by le- 
sions of the thalamus, 
for in all instances where 
this may have been the 
case the motor paralysis 
may also have been a re- 
sult of damage to neigh- 
boring parts (peduncles, 
internal capsule). 

Better founded is the 
idea that lesions of the 
pulvinar, the posterior 
part of the thalamus, 
give rise to defects in 
sight — crossed amblyo- 
pia or homonymous bi- 
lateral hemianopia — but 
the possibility that the 



inner) capsule 
is either direct- 
ly or indirectly 
implicated, we 
have a hemi- 
plegia which is 
either transient 
or persistent, ac- 
cording to the 
nature of the le- 
sion in the cap- 
sule. Whether 
the lenticular or 
the caudate nu- 
cleus alone is dis- 
eased can not be 
determined from 
the symptoms, 
that lesions of the thalamus, espe- 




f/B/ffS orrf/fy 
coRom 

RAD/ATA 

GOWSTO THCj 

OFT/C 

Jn/MMUS 




/f//Syf 

fiFTML4Mt/S\ 

Fig. 57- 
Figs. 54-57. — So-called " Frontal Sec- 
tions" through the Brain. Fig. 54, through 
the anterior commissure. Fig. 55, in front of the 
middle commissure. Fig. 56, behind the middle 
commissure. Fig. 57, immediately behind the chi- 
asm. The radiating fibres are shown diagrammat- 
ically in the last illustration. (After Edinger.) 



196 



DISEASES OF THE BRAIN PROPER. 
PITRES-NOTHNAGEL'S FRONTAL SECTIONS. 



Designation. 


Points where sections are 
made. 


Called by Pitres— 


Comprises, according to 
Nothnagel— 


A 


Immediately in front of 
genu of corpus callo- 
sum. 


Coupe prefrontale. 


Centri ovalis pars frontalis 
anterior. 


B 


Starting at the beginning 
of fissure of Sylvius. 


Coupe pediculo-^ 
frontale. 


Pars frontalis media. 


B, 


Between anterior cen- 
tral and frontal con- 
volutions. 


Pars frontalis posterior. 


C 


Through the fissure of 
Rolando. 


Coupe frontale. 


Pars centralis anterior. 


D 


Through ascending parie- 
tal convolution. 


Coupe parietale. 


Pars centralis posterior. 


E 


Through parietal lobe 3 
cm. posterior to the 
fissure of Rolando. 


Coupe pediculo-pa- 
rietale. 


Pars parietalis. 


F 


Through occipital lobe. 


Coupe occipitale. 


Pars occipitalis. 




Fig. 58.— Points at which the Pitres-Nothnagel's Sections are made. They all 
run parallel with the fissure of Rolando. 

posterior part of the optic tract is interrupted can even then 
not be excluded. The athetoid movements and symptoms of 
motor irritation (hemichorea, posthemiplegic tremor, athetosis) 
are, even if a connection actually exists between them and 
lesions of the thalamus (Greif, cf. lit.), certainly not character- 
istic of such lesions. The same holds good for the disturb- 



PITRES'S SECTIONS. 



[ 9 7 



ances in the muscular sense which have been observed in dis- 
eases of the thalamus (Meynert, Jackson). The relation finally 
between these latter and loss of the movements of facial expres- 



Section A. 




Fig. 59- — !. 2 i 3> nrst > second, and third frontal convolutions, 
centrum semiovale. 



prefrontal fasciculus of the 



sion in the course of central facial paralysis (von Bechterew) 
has been spoken of in Part II, Chapter V. 

Lesions of the internal capsule produce symptoms, varying 

Section B. (Bj Nothnagel.) 





Fig. 60. — 1 and 2, first and second frontal convolutions. 3, middle pediculo-frontal fasciculus. 
4, corpus callosum. 5, nucleus caudatus. 6, internal capsule. 7, lenticular nucleus. 8, 
island of Reil. 9, 10, n, superior, middle, and inferior frontal fasciculi. 

according- as the anterior or posterior limb is attacked. Pure 
capsular lesions — i. e., those in which the caudate as well as the 
lenticular nucleus remain intact — have rarely if ever occurred. 



DISEASES OF THE BRAIN PROPER. 
Section C. 




Fig. 61. — i, first frontal convolution. 2, 3, 4, superior, middle, and inferior frontal fasciculi. 
5, corpus callosum. 6, nucleus caudatus. 7, optic thalamus. 8, internal capsule. 9, 
lenticular nucleus. 10, claustrum. 

Fissures have been occasionally known to occur without having 
necessarily produced any motor disturbances in life (cf. Noth- 

Section D. 




Fig. 62. — 1, anterior central convolution. 2, corpus callosum. 3, caudate nucleus. 4, optic 
thalamus. 5, internal capsule. 6, island of Reil. 7, lenticular nucleus. 8, external 
capsule. 9, temporal fasciculus. 10, 11, 12, superior, middle, inferior parietal fasciculi. 



PITEES'S SECTIONS. 



199 



nagel, loc. cit., page 272). The functions of the anterior limb of 
the internal capsule are obscure, and lesions of this part do not 
produce any symptoms. With the posterior limb we are better 




Fig. 63.— 1, superior parietal fasciculus. 2, corpus callosum. 3, inferior parietal fasciculus. 
4 and 6, caudate nucleus. 5, optic thalamus. 

acquainted, and, above all, is this one fact well established, 
that a lesion of the anterior two thirds of the posterior limb 
gives rise to the usual typical hemiplegia, with paralysis of the 




Fig. 64.— 1, occipital convolutions. 2, occipital fasciculus of the centrum semiovale. 

Figs. 59-64. — Pitres-Nothnagel's Sections, the position of which is made clear by the 

table on p. 196. 

lower facial branches. A very small lesion at the knee may 
produce an isolated facial paralysis. If the posterior portion 
of the anterior two thirds is the chief seat of the disease, the 



200 



DISEASES OF THE BRAIN PROPER. 



paralysis is best marked in the leg. The posterior third of the 
posterior limb is occupied by the sensory fibres {le carrefour 
sensitif of Charcot), and lesions of that region cause a loss of 
sensation on the opposite side of the body (" hemianesthesia "), 
in which often the nerves of special sense are implicated, and 
hearing, smell, and taste (on the anaesthetic side) are, if not lost, 
at least diminished. Often hemiplegia is accompanied by hemi- 
anaesthesia, because if the one portion of the capsule is affected, 
an indirect and transitory implication of the other may occur. 
Usually such a hemiansesthesia soon disappears in the same 



Corp. genie. 

Ant. corpora med. 
quadrigemina 

I Brachium 
Aquaeductus\ of corpus 
1 quadri- 




Post. longitud. bundle 



Substantia 



Red nucleus 



nigra 



Fig. 65. — Diagrammatic Cross-section through the Anterior Corpora Quadri- 
gemina. (After Edinger.) 

way as the indirect motor disturbance often soon passes off in 
cases of persistent hemianassthesia. Whether the symptoms of 
motor irritation (the so-called post-hemiplegic chorea, for in- 
stance), which are a not rare accompaniment of hemiplegia, 
are due to disease of the internal capsule or to disease of the 
neighboring basal ganglia is as yet undecided. 



By the corpora quadrigemina we mean that peculiar eminence 
which by a crucial furrow is separated into four parts (bodies), and 
forms the posterior boundary of the third ventricle. In front it is 
bounded by the commissure which unites the two thalami ; on it 
rests the pineal gland (conarium). The anterior pair of bodies, 



THE CORPORA QUADRIGEMINA. 



20 1 



which are called the nates, are larger than the posterior, the testes. 
The appearance and structure, which these two pairs of bodies 
present in the lower mammals, justifies the conclusion that they 
are totally different from each other. Above the corpora quad- 
rigemina is situated the splenium of the corpus callosum ; be- 
tween the two is the transverse fissure of Bichat (the fissura 
choroidea). 

The frontal section through the anterior pair of the corpora 
quadrigemina (Fig. 65) shows the three divisions — the crusta, teg- 
mentum, and quadrigeminal ganglia. Toward the outer side is the 



Ventr. 




^^^^ 







Fig. 66.— Longitudinal Section through the Region of the Corpora Quadri- 
gemina of a Human Fcetus Twenty-eight Weeks Old. (After Edinger.) Shows 
that the posterior longitudinal bundle terminates in the nucleus of the oculo-motor nerve. 



pulvinar, with the lateral geniculate body. Emerging below the 
pulvinar is the crus, which contains the pyramidal tract (cf. page 
188). Between it and the tegmentum, in which is seen the red 
nucleus, is situated the substantia nigra. Below the aqueduct are 
the root fibres of the motor oculi, and in characteristic transverse 
section the posterior longitudinal bundle. The position of the lat- 
ter is made still clearer in the longitudinal section represented in 
Fig. 66. 

The manner in which the fibres from the red nucleus pass under 
the posterior pair of the corpora quadrigemina toward the middle 
line and then decussate with the fibres of the opposite side — the so- 
called " crossing of the brachia conjunctiva " (sup. peduncles of the 
cerebellum) — is represented in Fig. 67. 



202 



DISEASES OF THE BRAIN PROPER. 



Isolated lesions of the corpora quadrigemina are almost 
as rare as similar lesions of the capsule ; nearly always neigh- 
boring structures are implicated. The data which we pos- 
sess in this connection seem to indicate that lesions of the 
anterior pair produce visual disturbances, amblyopia, amauro- 
sis, and loss of pupillary reaction. Physiologically important 
is the fact that a root going to the optic tract is given off 




Fig. 67.— Diagrammatic Horizontal Section through the Decussation of the 
Superior Peduncles of the Cerebellum. (After Edinger.) 



from this anterior pair, and that radiating fibres pass to the 
nucleus of the third nerve, so that a connection exists be- 
tween stimulation of the optic nerve and stimulation of the 
oculo-motor (pupillary reflex) (Mendel). Authors seem to 
differ, however, about the extent to which this reflex is influ- 
enced by disease of the anterior pair of the corpora quadri- 
gemina. Impairment of certain movements of the eyes, espe- 
cially the upward motion of the ball, has been repeatedly 
noted by competent observers (Gowers). Nothnagel assumes 
that a lesion of the same oculo-motor branches on both sides, 
without the existence of an alternating paralysis of the ex- 
tremities, speaks for a lesion of the corpora quadrigemina (cf. 
loc. cit., p. 220). As to the function of the posterior pair of the 
corpora quadrigemina, all explanations are uncertain and hypo- 



LESIONS OF THE CRURA CEREBRI. 



203 



thetical. Baginsky assumed them to have a similar signifi- 
cance for the ear as the anterior pair for the eye, an idea in 
support of which further evidence is needed, and the disturb- 
ance of equilibrium which has been ascribed to disease of 
these bodies may well be produced by pressure upon the 
neighboring vermiform process of the cerebellum. On this 
point nothing positive is known. 

The crura cerebri emerge from the pons Varolii as two thick 
cylindrical white bundles of fibres ; on leaving it they diverge, 
having between them the posterior perforated space and the 




Lemniscus tract 

Pyramidal tract 

Fig. 68. — Sagittal Section through Pons and Medulla Oblongata. (After Men- 
del.) f, anterior commissure. p A , pulvinar. s, substantia nigra, r, tegmentum of 
crus cerebri. r 1} red nucleus, t, pes pedunculi. u, pons, v, hypoglossus nucleus with 
fibres emerging from it. a lT corpus quadrigeminum anterius. a 2 , corpus quadrigemi- 
num posterius. y, ansa lenticularis. S, Vicq-d'Azyr's bundle. A, optic tract. \ x , 
external thalamus-root of optic tract. A 2 , internal thalamus-root of optic tract, v, 
olivary body, o, anterior pyramid, t, posterior longitudinal bundle. Ic, locus caeru- 
leus. v. m, valve of Vieussens. m. b, Meynert's bundle, ad, abducens nucleus with 
emerging fibres. Bd, superior peduncle of cerebellum, oc, oculo-motor nucleus with 
emerging fibres. 



corpora albicantia (mammillaria s. candicantia). The situation 
of the crusta and the tegmentum (Fig. 69), and the masses of 
fibres contained in them, is once more shown in Fig. 68, which 
represents a longitudinal, sagittal section made almost in the 
middle line (r, tegmentum ; s, substantia nigra ; t, crusta). That 
the crusta forms the path for the voluntary, the tegmentum the 
path for the reflex movements, and that the latter also contains 
the sensory paths, as Meynert assumes, has not yet been proved 
by physiology. That the crusta, however, contains the motor 



204 



DISEASES OF THE BRAIN PROPER. 



path — namely, the pyramidal tracts — is a fact established beyond 
doubt ; hence its lesions will for the present be of more practi- 
cal interest. Only a small number of instances of lesions in the 
tegmentum have been reported. A case of Buss (cf. lit.) pre- 
sented ataxia of ail four extremities, anaesthesias, disturbances 
of the muscular sense, and an affection of the right hypoglossus. 
At the autopsy a focal lesion was found in the tegmentum of 
the crus and the pons. 

Considering: the relation which the third nerve bears to the 



median part of the crus cerebri, as is 



shown in Fig. 69, we 
can well understand 
that in lesions of the 
latter the oculo-mo- 
tor is not rarely im- 
plicated, and autop 
sies have frequently 
demonstrated that, 
wherever an oculo- 
motor paralysis has 
been associated with 
paralysis of the ex- 
tremities on the op- 
posite side, the le- 
sion is situated in the 
crus cerebri. For 
example, in a pa- 
Fig. 69. — Cross Section through the Region of the +i en f with OCulo-ttlO- 
Ant. Corpora Quadrigemina. . 

... , tor paralvsis of the 

qn.a. anterior corpora quadrigemina ; g.c. gray matter around _ . 

the aqueduct of Sylvius; ag, aqueduct of Sylvius; nlll right side and hemi- 
nucleus of the third nerve ; ///. posterior longitudinal bun- r)lecna of the left side 
die; r. k. red nucleus (tegmentum) ; sn, substantia nigra ,. ( 7^ . 
(locus niger) ; /, cerebral peduncle. V 1 * DOth. COme On at 

the same time !), we 
may without hesitation diagnosticate a focal lesion in the right 
crus cerebri ; if, in addition, anaesthesia exists on the para- 
lyzed side, an implication of the tegmentum must be sus- 
pected. 

The pons Varolii, which connects the two hemispheres of 
the cerebellum, contains, as we said above (cf. page 78), the 
nuclei for several nerves and the fibres passing from them to 
the brain. The nuclei, which are situated in the upper seg- 
ment, are those of the fifth, the facial, and the abducens. Since 
the pons naturally also contains the motor fibres, situated, as 




LESIONS OF THE PONS. 



205 



we said above, in the lower or ventral segment, while in its 
dorsal part one meets the sensory bundles, pontine lesions may 
produce a complication of symptoms as characteristic as those 
produced by lesions in the crus. As we have attempted to 
make clear in Fig. 70, the fibres of the facial nerve decussate 
higher up than the motor fibres of the pyramidal tracts. Keep- 
ing this fact in mind, we can easily understand that a lesion of 
the lower part of the pons concerns the 
facial fibres after their decussation, the 
fibres going to the extremities, however, 
before they cross, and consequently gives 
rise to a facial paralysis on the side of 
the lesion, but a paralysis of the extremi- 
ties on the opposite side (hemiplegia 
alternans) (Gubler, 1859). A lesion of 
the upper part of the pons concerns both 
of these paths before their decussation, 
and produces, therefore, hemiplegia, 
with a facial paralysis of the same side, 
which, however, is distinguished from 
the typical hemiplegia in that the facial 
paralysis in our case resembles some- 
what the peripheral type, as it takes in 
all three branches of the facial, and as, 
though but rarely, reaction of degenera- 
tion may be present (cf. page 84). 

If, then, we meet with a paralysis 
which affects the facial on one, the ex- 
tremities on the opposite side (alternat- 
ing paralysis), simultaneously, we are 
justified in assuming the lesion to be 
situated in the pons, and more especially 
in its lower part. If paralysis first oc- 
curs in the face alone, and does not de- 
velop in the extremities until later, and 

if the whole process is gradual, it may arise from a tu- 
mor at the base of the brain. If, besides the symptoms 
described, the patient complains of pain in the face, the 
trigeminus is included in the lesion. A paralysis of the 
external rectus points to the implication of the abducens 
nerve, in which case a paresis of the internal rectus of the 
other side not rarely co-exists, so that a conjugate deviation 




Fig. 70.— Diagram showing 
the Decussation of the 
Fibres going to the 
Extremities, and of 
those going to the 
Face, in the Pons and 
Medulla Oblongata. F, 
facial fibres. E, fibres go- 
ing to the extremities. P, 
pons. O, medulla oblon- 
gata, pyx, decussation of 
the pyramidal tracts, a, a 
focus in the upper, b, a 
focus in the lower part of 
the pons (the latter is situ- 
ated below the decussation 
of the facial fibres). 



206 



DISEASES OF THE BRAIN PROPER. 



of the eyeballs toward the paralyzed side — that is, away from 
the focus — may occur. 

Bilateral lesions of the pons must be thought of in combined 
paralyses of the extremities and cranial nerves, or in cases of 
bilateral facial paralysis or bilateral paralysis of the extremities 
(either of both legs or of all four extremities). The diagnosis, 
however, as a rule, can not be made with certainty. 

Convulsions will be observed if by acute lesions the spasm 
centre, as Nothnagel calls it, becomes excited. Tonic spasms 




Fig. 71. — The Cerebellum seen from Behind (dorsal aspect). 



in the paralyzed limbs are not uncommon. Psychical changes, 
which occur in connection with lesions in the pons, are very 
irregular in their occurrence, and assume the most diversified 
forms. They deserve a more careful study than has as yet 
been devoted to them. Their entire absence has been repeat- 
edly noted. Anaesthesias in the distribution of the trigeminus, 
as well as in the extremities, are comparatively frequent, but 
we are not at present able to utilize them for the purpose of 
topical diagnosis. 



THE CEREBELLUM. 



207 



The small brain — cerebellum — is made up of a middle part, the 
so-called vermiform process, and two lateral parts, the hemispheres. 




Fig. 72.— Cerebellum seen from in Front (ventral aspect). Vel. m. a. , valve of Vieus- 
sens. Binde A, superior peduncle of cerebellum. 

Fig. 71 represents the superior (the upper, posterior, dorsal aspect), 
Fig. 72 the inferior vermiform process (the lower, anterior, ventral 




Fig- 73- — The Connections of the Cerebellum— with a, the midbrain (superior pe- 
duncles), 5 ; &, the pons (middle peduncles), 7 ; c, the medulla oblongata (inferior pedun- 
cles or restiform bodies), 3. 1, fourth ventricle. 2, stria? acusticse. 4, funiculi graciles. 
6, lemniscus. 8, corpora quadrigemina. 



aspect), with the various portions of the hemispheres. The cere- 
bellum is connected with the corpora quadrigemina by the superior 



208 



DISEASES OF THE BRAIN PROPER. 



peduncles of the cerebellum, with the pons by the middle peduncles, 
the processus e cerebello ad pontem, and with the medulla oblongata 
by the inferior peduncles or restiform bodies. The situation of these 
arms or brachia is shown in Figs. 73 and 75. 



To enable us to point with certainty to the cerebellum as 
the seat of disease, the implication of the vermiform process is 
necessary, since, as Notbnagel has pointed out, we may have 
extensive disease in the hemispheres without the manifestation 
of a single symptom during life. In the cases, however, in 
which the vermiform process is affected, marked disturbances 

of co-ordination and equilibrium 
ensue ; the patient staggers and 
complains of severe vertigo on 
walking and standing. This 
is almost a pathognomonic 
symptom, especially if it be as- 
sociated with occasional spells 
of more or less serious vomiting, 
when the name " cerebellar " is 
not improperly applied to it. 
Of course we must also keep 
in mind, if such symptoms are 
remarked, that something simi- 
lar occurs in other diseases, es- 
pecially in Meniere's disease, 

for 
additional points before exclud- 
ing these. This is, however, 
not always easy, and often 
enough — for instance, if vomiting occurs without vertigo — 
the diagnosis must remain open. If, on the other hand, the 
change in the walk of the person is so pronounced that it can 
be easily confounded with that of a drunken man, the ques- 
tion is easier to solve. 

Acute lesions of the middle peduncles of the cerebellum 
produce highly characteristic symptoms, so that a diagnosis 
can be made with a fair amount of certainty. The body is in- 
voluntarily gyrated around its longitudinal axis (" forced move- 
ment "). This symptom, however, can only be observed as a 
consequence of irritation of the peduncles, but is absent if the 
latter are wholly destroyed — e.g., by haemorrhage. Sometimes 




Fig. 74.— The Anterior (Lower) Sur- 
face of the Medulla Oblongata. 

With (1) the anterior pyramids; (2) the ^ must therefore ] 
decussation of the pyramids ; (4) the an- 
terior, (3) the posterior nerve-roots (the 
anterior median fissure has been widened 
by drawing the pyramids apart). 



THE MEDULLA OBLONGATA. 



209 



the patient has an irresistible inclination to lie on one side, and 
this is, if the remaining symptoms point in the same direction, 
also to be estimated as a forced movement, or rather a " forced 
position." It is not uncommonly accompanied by a corre- 
sponding twist of the head and eyeballs. This phenomenon, 
however, is not a pathognomonic symptom for lesions of the 
middle peduncles. The di- 
rection in which the body is 
turned is sometimes toward 
the diseased side, sometimes 
away from it, a fact for which 
no explanation has as yet been 
found. 

For lesions of the other 
peduncles of the cerebellum 
(the superior and inferior) no 
diagnostic points are known. 

The lowest part of the en- 
cephalon is called the medulla 
oblongata. It is continuous 
below with the spinal cord on 
a level with the lower margin 
of the foramen magnum. On 
its anterior (lower, ventral) as- 
pect we observe (Fig. 74) the 
pyramids with their decussation, 
the olives with the nucleus 
dentatus (Fig. 19), and to the 
outer side of these are to be 
found the restiform bodies, the 
inferior peduncles of the cere- 
bellum. The latter contain the so-called direct cerebellar tracts, 
which, coming from the outermost portion of the lateral col- 
umns in the cord, pass, through the anterior commissure of the 
vermiform process, to the cortex of the cerebellum. We shall later 
on have to refer to these tracts again. That a relation exists be- 
tween the olives and the cerebellum is apparent from the fact that 
wherever we have a congenital atrophy of the cerebellum these 
bodies are also atrophic (Flechsig). 

On the posterior (dorsal, upper) aspect is the floor of the fourth 
ventricle, the fovea rhomboidalis (Fig. 75), which is bounded below 
by the diverging restiform bodies, above by the diverging superior 
14 




Fig- 75-— The Posterior (Dorsal) Aspect 
of the Medulla Oblongata, i, poste- 
rior commissure. 2, peduncle of pineal gland. 
3, corpora quadrigemina. 4, superior pedun- 
cle. 5, middle peduncle. 6, inferior pedun- 
cle of cerebellum. 7, striae acusticse. 8, funic. 
te:es. 9, otex. 10, funiculi graciles. 



2io DISEASES OF THE BRAIN PROPER. 

peduncles of the cerebellum. The median columns are called the 
posterior pyramids (funiculi graciles). They are the continuations 
of Goll's columns of the spinal cord. To the tracts situated to the 
outer side of these the name funiculi cuneati, or Burdach's columns, 
has been given. 

To diagnosticate the medulla oblongata as the seat of a 
lesion is only possible if the nuclei in the floor of the fourth 
ventricle are diseased, in which case we get the clinical picture 
of the bulbar paralysis described on page 154. Other charac- 
teristic symptoms do not exist, and more especially it must not 
be forgotten that foci in the medulla may give rise to a paral- 
ysis only in the extremities, which presents nothing character- 
istic during life. If, however, the nerve nuclei of the medulla 
are implicated, a characteristic picture is presented which can 
hardly be mistaken. Another point of which, in making our 
topical diagnosis, we must not lose sight, is the fact that cer- 
tain brain lesions may give rise to a similar combination of 
symptoms constituting the clinical picture of the disease which 
we have described above as pseudo-bulbar paralysis. Other 
diseases of the medulla — traumatism, acute and gradual com- 
pression, haemorrhage, and embolism — are of no practical sig- 
nificance, since they cause death so quickly that a certain 
diagnosis is impossible. Hence we will pass them over with- 
out further remark. Of the tumors observed in the medulla 
oblongata we shall speak later. 

LITERATURE. 

Brissaud. Degenerations secondaires dans le pedoncule cerebral. Publications 

du Progr. med., 1879. 
Tomaszewski. Zur Pathologie des Grosshirnschenkels. Inaug. Dissert. Bres- 

lau, 1881. 
Greiff. Zur Localisation der Hemichorea. Arch. f. Psych, und Nervenkrankh., 

xiv, 3, 598 et seg., 1883. 
Senator. Zur Diagnostik der Herderkrankungen in der Eriicke und dem ver- 

langerten Marke. Arch. f. Psych, und Nervenkrankh., xiv, 3, p. 643 etseq., 

1883. 
Schrader. Ein Grosshirnschenkelherd mit secundaren Degenerationen der Pyra- 

mide und Haube. Inaug. Dissert. Halle, 1884. 
Bleuler. Zur Casuistik der Herderkrankungen der Briicke. Inaug. Dissert, aus 

Bern (Lichtheim). Leipzig, 1885. 
Meyer. Beitrag zur Lehre der Degenerationen der Schleife. Arch. f. Psych. 

und Nervenkrankh., xvii, 2, p. 439 et seq., 1886. 
Edinger. Deutsche med. Wochenschr., No. 14, 1886 (small focus in the centrum 

semiovale causing aphasia and bilateral paresis of the hypoglossus). 



PA THOLOGICAL DIA GNOSIS. 2 I I 

Jelgersma. Centralbl. f. Nervenheilk., ix, 16, 1886. 

Leube. Deutsches Arch. f. klin. Medicin, 40, 2, p. 217, 1887 (foci in the 
crus). 

Siemerling. Casuistischer Beitrag zur Localisation im Grosshirn (focus of soften- 
ing in the left occipital lobe, right-sided hemianopia). Arch. f. Psych., xviii, 
p. 877, 1887. 

Hun, Henry. A Clinical Study of Cerebral Localization illustrated by Seven 
Cases. Amer. Journ. of the Med. Sciences, January, 1887. 

Bechterew. Die Bedeutung der Sehhiigel auf Grund von experimentellen u. 
pathologischen Daten. Virchow's Archiv, Bd. 1 10, Heft 2, p. 322, 
1887. 

Buss. Ein Fall von acuter disseminirter Myelitis bulbi nebst Encephalitis bei 
einem Syphilitischen. Deutsches Arch. f. klin. Med., Bd. 41, Heft 3, Sep- 
tember, 1887. 

Spitzka. Deutsche med. Wochenschr., 8, p. 157, 1887 (focal lesion at the junc- 
tion of pons and medulla oblongata). 

Demange. Ataxie symptomatique (" hemiataxie bilaterale ") par lesions sym- 
metriques du cerveau. Revue de m£d., 2, 1888. 

Jastrowitz. Beitrage zur Localisation im Grosshirn und deren praktische Ver- 
werthung. Deutsche med. Wochenschr., 5 et seq., 1888 (tumors). 

Arndt. Zur Frage der Localisation der Functionen der Grosshirnrinde. Berl. 
klin. Wochenschr., 8, 1888. 

II. The Study of Cerebral Lesions with Reference to 
their Pathological Nature. 

Pathological Diagnosis.— -We have before pointed out that 
the question as to the nature of a brain disease is not only of 
interest to the physician, but of the greatest importance to the 
patient, as on this the prognosis as well as the mode of treat- 
ment turns. An error in the topical diagnosis may deserve 
the censure of scientific criticism, but does not necessarily en- 
tail damage to the patient. If, on the other hand, we mistake 
the nature of the lesion in a given case — if, for instance, a dis- 
ease of the vessels is taken for a new growth, if the tuberculous 
or syphilitic nature of the affection is overlooked, or, again, a 
severe alcoholic intoxication is diagnosticated where in reality 
an apoplexy exists — when such errors have influenced the treat- 
ment, not only opportunities may be lost for the patient which 
may never present themselves again, but an unfavorable event 
of the disease may actually be brought about or at least pre- 
cipitated. On these grounds we ought to be particularly care- 
ful and conscientious in forming this part of our diagnosis, 
and no symptom, however small it may seem, should be over- 
looked, as we never know but that it may later perhaps be- 
come of diagnostic value. 



212 



DISEASES OF THE BRAIN PROPER. 



Ill looking over the sevei'al pathological processes which 
here concern us, we find that their number is comparatively 
limited. First of all, we shall devote our attention to diseases 
of the blood-vessels, which so frequently are the cause of cere- 
bral lesions. We shall have to determine the nature of these 
diseases and carefully distinguish the affections of the blood- 
vessels from the secondary changes produced by them. The 
clinical symptoms, the complaints of the patient, and the ob- 
jective signs are a direct consequence of the latter only, and 
it is therefore not the disease of the blood-vessels which we 




Fig. 76.— Diagram showing the Circle of Willis. The carotids with the anterior 
and middle cerebral arteries and the basilar with the posterior cerebrals are connected by 
communicating branches. 



have practically to deal with, but the changes in the brain sub- 
stance which they entail. The clinical manifestations vary 
according to the seat of the diseased vessel and the portion of 
the brain supplied by it. The symptoms we shall describe in 
detail later ; but first let us speak of the pathological nature of 
the diseases of the cerebral vessels. 



THE CEREBRAL VESSELS. 



213 



AFFECTIONS OF THE BRAIN DUE TO DISEASE OF THE 
BLOOD-VESSELS. 

A. Diseases of the Cerebral Vessels and their Conse- 
quences. — The arteries of the brain are derived from the internal 
carotids and the basilar, which is formed by the two vertebrals. 
The internal carotid gives off two terminal branches, the anterior 
cerebral (arter. corpor. callos.) and the middle cerebral (arter. foss. 
Sylv.). The basilar divides into the two posterior cerebrals (arter. 
profund. cerebri). These receive on each side a communicating 
branch from the internal carotid, the so-called posterior communi- 
cating artery, and the two anterior cerebrals are connected by an 
anterior communicating branch, so that a closed circle (or rather a 




Fig- 77-— The Cortical Distribution of the Middle Cerebral Artery. (After 
Charcot.) From left to right the five branches are named as follows: The inferior 
frontal branch to Broca's convolution, the ascending frontal branch, the ascending parie- 
tal branch, the parieto-sphenoidal, and the sphenoidal branches. 



heptagon, according to Hyrtl) of arteries is formed, known as the 
circle of Willis, an arrangement which is of the last importance for 
the distribution of the blood in the brain (cf. Fig. 76). 

The fact that the left carotid comes off from the aorta nearly in 
a straight line with the blood-current in the arch, while the innomi- 
nate, which gives off the right carotid, leaves the aorta almost at 
right angles, easily explains the greater frequency of embolism on 
the left side. A somewhat similar condition exists in the vertebrals, 
where the left, often the larger one, arises from the subclavian at its 
highest point. This is, however, of less moment for cerebral lesions, 



2i 4 DISEASES OF THE BRAIN PROPER. 

as the blood has first to pass the basilar before entering the brain 
substance. 

Of the three before mentioned arteries — the anterior, middle, and 
posterior cerebrals — each one supplies two sets of vessels totally dis- 
tinct from each other — namely, first, the so-called cortical arteries ; 
secondly, the arteries of the basal ganglia. The important difference 
between these two systems consists in the fact that the former, as 
Heubner and Duret have shown, possess anastomoses, while the lat- 
ter are, as they have been called by Cohnheim, terminal arteries — 
that is. they do not communicate with each other, but pass directly 
into the capillaries. The significance of such an arrangement is ap- 




Fig. 78. — Frontal Section through the Cerebral Hemispheres, One Centime- 
tre behind the Chiasm. Shows the distribution of the middle cerebral artery in the 
lenticular nucleus. 



parent, and we shall not be surprised to find that occlusion of an 
artery of the second set almost always produces death of the parts 
supplied by it. 

Of the three cerebral arteries, the middle, the Sylvian artery, has 
by far the widest distribution and is the most important; for while 
the anterior supplies the corpos callosum, the gyrus rectus, the para- 
central lobule, and the precuneus; the posterior, the crus, the tem- 
poral, and the occipital lobe, and the cuneus, sending also a few 
branches to the optic thalamus (arter. optic, posterior.), it remains 
for the middle cerebral to supply the whole lenticular and the cau- 
date nucleus, and, above all, the internal capsule. Moreover, the 
central and cortical motor region, the cortical areas concerned in the 
process of speech (on the left side), the cortical centre for hearing, 
probably also for vision, depend on this artery for their nutrition. 

Its cortical distribution, its subdivision into the frontal, parie- 



CERE BR A L HALMORRHA GE. 



215 



tal, parietosphenoidal, and sphenoidal arteries, is made clear by 
Fig. 77. 

Its distribution to the lenticular nucleus is illustrated in Fig. 78. 
The internal artery of the corpus striatum, also called the lenticular 
artery, goes to the first and second segment of the lenticular nucleus, 
while the external branches are the so-called lenticulo-striate and 
lenticulo-optic arteries. Among the former, the one which supplies 
the third segment of the lenticular nucleus, the upper portion of the 
internal capsule, and the caudate nucleus deserves special mention. 
It is so frequently the seat of haemorrhage that Charcot has called it 
" I'arfere de V 'hemorrahagie cerebrate." 

The 'tween-brain and the mid-brain are mostly supplied by the 
posterior communicating and its branches, the cerebellum by several 
so-called cerebellar branches (arter. cerebell. super, et infer.) com- 
ing from the vertebrals; the pons and medulla oblongata also by 
branches of the vertebrals, which are the so-called rami ad pontem 
and rami ad medullam oblongatam. For details the reader is re- 
ferred to Duret. 

The internal carotid and the basilar measure 4 mm. in diameter; 
the vertebrals, 3.5 mm. (Luschka). The blood pressure in the carotid 
is generally taken to correspond to from 140 to 160 mm. Hg. How 
guarded, however, we ought to be in accepting such statements has 
been shown by Loewenfeld, who drew attention to the variations in 
the development of the cerebral arteries; and it seems at least pos- 
sible that this is of considerable aetiological significance for different 
cerebral affections (Loewenfeld, Arch. f. Psych, und Nervenkrankh., 
Bd. xviii, 3, page 819, 1887). 

1 . Cerebral Hemorrhage, Hcemorrhagia Cerebri {Periarteritis 
Cerebralis, Miliary Aneurisms of the Cerebral Arteries). 

Pathological Anatomy and ^Etiology. 

Of all cerebral affections, haemorrhage, the result of the rupt- 
ure of a vessel, is by far the most important and the most fre- 
quent. As we should expect, haemorrhages of various kinds may 
be produced by traumatism (injury to the skull, with or without 
fracture). They may occur between the inner side of the skull 
and the loosened dura mater, or in the sac of the dura or that 
of the pia (submeningeal hasmorrhage) ; but, disregarding these, 
there is one affection especially which gives rise to cerebral 
haemorrhage — namely, a diffuse periarteritis — which was first 
described by Charcot and Bouchard in 1868. In this process 
a thickening of the lymph-sheaths, and consequent changes in 



2l6 



DISEASES OF THE BRAIN PROPER. 



the muscularis take place, by which the formation of miliary 
aneurisms is favored (cf. Figs. 79 and 80). Rupture of these 
aneurisms then gives rise to hemorrhages, and so frequently 
is this the case that the authors before mentioned found this 




Fig. 79. — Cerebral Artery from an Apoplectic Focus, ma, miliary aneurism, ble, 
extravasations of blood into the adventitial lymph space. (After Cornil and Raii- 
vier.) 



condition in every one of seventy-seven consecutive cases which 
came under their observation. 

For the rupture of these aneurisms it is by no means al- 
ways necessary to have any extraordinary exciting cause, such 
as an elevation of the blood pressure, which may temporarily 
be produced by bodily exertion, sneezing, coughing, vomiting, 

and the like, or which may 
permanently exist where the 
heart is bypertrophied, as 
in valvular disease or in 
cases of contracted kidney. 
In many of the instances 
nothing of the kind can be 
demonstrated. 

The size of the aneurism varies from 0.2 to 1 mm. ; their 
color and consistence often differ greatly. Their favorite seat 
is in the thalamus, the corpus striatum, the convolutions, and 
the pons, while they are less frequently met with in the cen- 
trum ovale, the crura, and the medulla oblongata. Sometimes 
only two or three, at other times as many as several hundred, 




Fig. 80.— Miliary Aneurism of a Small Ar- 
tery of the Lenticular Nucleus. (After 
Marchand.) 



CEREBRAL HEMORRHAGE. 



217 



have been detected in one brain. On being squeezed they are 
found to contain white corpuscles, fat droplets, and amorphous 
granular masses. 

The haemorrhage which is produced by their rupture con- 
sists when fresh of a dark- colored loose coagulum. The wall 
of the " focus " is red and spotted with punctiform haemor- 
rhages (capillary apoplexies), and presents a ragged and torn 
appearance. Gradually the dark color becomes lighter, the 
neighboring parts become infiltrated, yellowish, and very soft 
(lemon-colored oedema). As a rule, the focus becomes later en- 
capsuled by a layer of neuroglia, the fibrin masses become 
mixed with the debris of the nerve elements, and we get a 
smooth-walled cavity with liquid contents, the so-called apo- 
plectic cyst, occupying a smaller space than the original 
haemorrhage. If the walls approach each other before the 
coagulum is transformed, a great increase of fibrillated con- 
nective tissue takes place and we get a so-called apoplectic 
scar. 

The effect of the haemorrhage varies according to its posi- 
tion, according to the calibre of the ruptured vessel, upon 
which depends its amount, and according to the rapidity or 
slowness with which the blood escapes. The favorite seat for 
haemorrhages is in the large ganglia (Charcot, Andral, Ro- 
choux) ; with decreasing frequency they are found (Noth- 
nagel) in the remaining portions of the cerebral hemispheres, 
much more rarely in the pons and the cerebellum. The fre- 
quency is directly influenced by the size of the different cere- 
bral vessels and by the blood pressure. The diameter of the 
vessels of the brain stem is considerably larger than that of 
those going to the cortex. The above-mentioned " artery of 
cerebral haemorrhage " is of an especially large calibre (i x / 2 to 2 
mm.), and causes therefore when it bursts a particularly large 
and extensive haemorrhage, because the bleeding is prolonged. 
" The traumatic effect of the haemorrhage," as Wernicke calls 
it, is equal to the product of the mass of effused blood into the 
square of the rapidity with which it is poured out, which latter 
depends directly upon the blood pressure in the vessels. Hence 
it follows that, as regards the effect of a haemorrhage, the 
blood pressure is of more importance than the calibre of the 
vessel. 

./Etiology. — In examining into the aetiological factors con- 
cerned in a cerebral haemorrhage, we must distinguish those 



2I g DISEASES OF THE BRAIN PROPER. 

which produce the disease of the vessels from those which 
directly cause the haemorrhage ; in other words, the predis- 
posing from the exciting causes. 

About the former not much is known ; nevertheless, con- 
siderable influence in the causation of arterial disease must be 
ascribed to age, as we can not deny that it is decidedly less 
frequently to be observed in the young than in older persons, 
and that the smallest percentage of apoplexies is found between 
the fifth and thirtieth years of life. Still, to lay so very much 
stress upon the significance of age is not warranted by experi- 
ence. The fact that cerebral haemorrhage is by no means rare 
in people from twenty to thirty years old clearly shows that 
miliary aneurisms may occur even at a comparatively early 
period of life, nor are these cases by any means always those of 
persons laboring under hereditary disadvantages, since even 
members of perfectly healthy families who are yet young may 
fall victims to a stroke of apoplexy. The influence of heredity 
as well as that of age has undoubtedly been overrated in this 
connection. It is true there are families in which apoplexy 
seems to be a natural occurrence, but such instances are excep- 
tional, while on the other hand the arterial disease develops in 
an infinitely larger proportion of cases apparently without 
special hereditary cause. Sometimes the development of the 
disease seems to be favored by a peculiar " habitus." So, cor- 
pulent individuals of medium height, with short necks, broad 
thoraces, who on the least exertion or excitement become pur- 
ple in the face, have usually been looked upon as particularly 
predisposed to apoplexy, and in many cases with justice, yet 
those who have in an extensive practice seen how often tall, 
spare individuals with narrow chests die from cerebral haemor- 
rhage, will readily give up the idea that an apoplectic habitus 
is a conditio sine qua non. 

The role which sex plays can not be denied. The disease is 
much more frequently observed in males than in females, while 
with embolism, as we shall see, the reverse is true. To explain 
this predisposition in males, other factors — namely, the mode of 
life — must, I think, be taken into account, and here it is, in the 
first place, the occupation, and, secondly, the abuse of alcohol, 
which must be considered. Notwithstanding the fact that we 
know very little about the influence of occupation on the for- 
mation of miliary aneurisms, our statistics of fatal cases of cere- 
bral haemorrhage in the different trades being somewhat unre- 



ETIOLOGY OF CEREBRAL HAEMORRHAGE, 2 IQ 

liable, still we have some sure grounds, the correctness of 
which can scarcely be called in question. That, for instance., 
the working in certain poisons, especially in lead, predisposes 
to arterial disease, and consequently to apoplexy, is indisputa- 
ble. In his thesis on encephalopathia and arthralgia saturnina, 
prepared under my auspices, Schulz (Breslau, 1885) points out 
the frequency of the so-called hemiplegia saturnina, and calls 
attention to the fact that Berger has made similar observations. 
Later on, in our consideration of lead poisoning, we shall have 
to refer again to this subject, and discuss the probable action 
of the metal on the nervous system. In the second place, those 
who are exposed to radiating heat — workers at furnaces, pud- 
dlers— are in danger, especially if their work is connected with 
much bodily exertion, and this can hardly surprise us if we 
remember how much circulatory disturbances are favored by 
such circumstances. The same may be said of occupations 
which necessitate uncomfortable positions of the body, as, for 
instance, is the case in agate polishers, who constantly have to 
lie on their abdomens, or in coal miners, who have to remain in 
a stooping position all the time. 

In regard to the abuse of alcohol we refer not only to the 
confirmed drunkards, but much rather to that class of indi- 
viduals who habitually consume more alcohol, especially beer, 
than is good for them. Such men rarely, if ever, get drunk, 
but they drink several times a day one or two glasses of beer, 
do not take enough exercise, and become fat and predisposed 
to fatty heart and arterial disease, especially arterio-sclerosis, 
which affection, we may say finally, is the real cause of the 
greater frequency with which apoplexy is met with in men 
than in women. The fatty heart may be present even without 
any marked obesity. 

The important influence of syphilis in the origin of cerebral 
haemorrhage is proved by many irrefutable observations, and, 
considering the part played by it in disease of the cerebral 
vessels, this can easily be explained. We shall mention it 
again in this chapter, and later dwell more particularly on the 
symptoms peculiar to the syphilitic hemiplegia. Exceptionally, 
hemiplegia occurs after diphtheria, sometimes in conjunction 
with a paralysis of the palate, sometimes independently. In a 
girl aged fifteen under my care, hemiplegia developed fourteen 
days after diphtheria without any simultaneous disturbance of 
consciousness, and only slight improvement was noticed after 



220 DISEASES OF THE BRAIN PROPER. 

several years. With equal rarity is this complicating sequela 
found after other acute diseases — for instance, scarlatina. 

Sometimes no exciting cause can be demonstrated, but if 
such be observed, they are always associated with a sudden 
more or less marked increase of the blood pressure. People 
with diseased cerebral vessels are not rarely suddenly attacked 
by an apoplectic stroke on a strong emotion, hard bodily exer- 
tion, during violent attacks of coughing, sometimes also in a 
cold bath and after a full meal. 

How it comes about that the coldest months of the year 
yield the largest percentage of victims to apoplexy, and why it 
is that in the twenty -four hours there are two periods with a 
maximum and a minimum death-rate, if such be actually the 
case, can not be explained. Such has, however, been claimed 
by Sormani, who based his statements upon an extensive study 
of statistics (Riv. clin., ser. 2, i, 12 Dicembre, 1871). The same 
author also is inclined to attribute to the position of the ba- 
rometer some influence on the mortality, as in his opinion sud- 
den changes in the weather materially increase the mortality 
from apoplexy. 

Symptoms and Course. — The rupture of a fair-sized cere- 
bral vessel is always, no matter what part of the brain is affected 
by it, attended with more or less violent symptoms. 

Only in exceptional cases is it preceded by premonitory in- 
dications. Occasionally there are temporary sensory disturb- 
ances in the extremities of one side, formication, numbness, a 
feeling of heaviness in the limbs, pain in the soles of the feet, 
certain choreiform movements in the face and arms (hemicho- 
rea prashemiplegica, Raymond), symptoms which indicate that 
things are not going in their usual order. The patient may 
also complain of headache and a feeling of fullness in the head, 
which makes itself manifest on the least provocation, on the 
slightest emotion, or after a small amount of wine has been 
taken. But rarely enough are such premonitions sufficiently 
appreciated by the patient, and only too often are they incor- 
rectly interpreted by the physician. Usually they are over- 
looked, and are first remembered when the catastrophe is 
either imminent or has already taken place. 

When the attack does come on, the patient gradually or 
suddenly loses consciousness, and remains in this condition for 
a few minutes, hours, or even for a day or two, according to 
the severity of the "stroke." The higher the blood-pressure, 



THE APOPLECTIC ATTACK. 221 

and the greater the rapidity with which the blood escapes, the 
more pronounced and severe are the general symptoms, which 
collectively are called " apoplectic stroke " (the " insult " of the 
Germans). The way in which the disturbance of conscious- 
ness comes on varies very widely in different cases. Thus one 
patient may for some hours before the actual attack present a 
peculiar excitement, he is restless and bewildered, may even 
have forgotten the ins and outs of his own house, his speech is 
agitated, etc. Another patient may complain of headache and 
vertigo ; a third, of a feeling of heat in his head and of general 
prostration (" different forms of delayed stroke "). All these 
premonitory symptoms which we have described may, how- 
ever, be absent, and a person apparently enjoying the best of 
health may suddenly, as if "struck by lightning," sink to the 
ground and lie there unconscious {apoplexie foudroyante). 

If we are called to such a case, the following conditions will 
present themselves to us on our first examination : The patient 
lies on his bed as if asleep, his respiration is either quiet and 
deep or loud and stertorous, he can not be aroused in any way, 
not even by strong irritation of the skin (pricking, tickling), his 
eyes are closed and the pupils, usually of medium size, neither 
much dilated nor much contracted, have lost their power to 
react. With every expiration the cheeks are slightly puffed 
out, and it is often soon apparent that one corner of the mouth 
is lower than the other. The extremities are relaxed, and when 
raised drop loosely. The tendon reflexes are absent in severe 
cases and neither the cremasteric nor the plantar reflex can be 
obtained. The pulse is full, somewhat slow ; the temperature 
normal, perhaps slightly subnormal ; the urine presents no 
changes, or may contain a trace of albumen, rarely of sugar. 

This condition may, as we have said before, last several 
minutes, several hours, or even one or two days. It is modi- 
fied gradually according as the haemorrhage sooner or later 
comes to a stop or continues without interruption until a fatal 
result ensues. In the former case the patient gradually begins 
to react to strong stimuli, and may open his eyes for a short 
while, when called loudly or when water is thrown over him ; 
he may give a loud yawn and show some voluntary motion of 
the extremities. Gradually consciousness returns, and the 
patient attempts to make himself understood by gestures and 
words, and in the most favorable instances, which are, how- 
ever, unfortunately very rare, the physician can feel assured 



222 DISEASES OE THE BRAIN PROPER. 

that everything has cleared up, that the patient is again in pos- 
session of perfect consciousness, of the power of speech, and of 
motion. In such cases we speak of a " stroke without focal 
symptoms." 

But the bleeding may continue, although only under low 
pressure, and only cease very gradually ; then the symptoms 
abate but slowly and the recovery is only partial ; the patient 
lies for days in a state of somnolence, and repeated examina- 
tions show that one corner of the mouth is distinctly lower 
than the other, and that the saliva dribbles from, it involunta- 
rily. If we can, by strong stimuli, evoke spontaneous move- 
ments, it becomes evident that only one side is moved, that only 
one arm or one leg is raised, while the other side remains per- 
fectly motionless, and after consciousness is fully restored the 
certainty is forced upon us that one side of the body is de- 
prived of its power, or, as we say, is paralyzed. This we call 
a " stroke with focal symptoms." 

Again, the haemorrhage may not cease at all, but continue 
with increased blood-pressure ; then the patient remains un- 
conscious, the breathing becomes irregular and more rapid, 
and assumes the so-called Cheyne-Stokes' type, the pulse be- 
comes more rapid and small in volume, the face grows pale 
and haggard, the saliva getting into the trachea produces the 
well-known tracheal rattling, the temperature rises gradually 
but noticeably, and the patient dies without having come to 
himself, and after a period of unconsciousness which may have 
lasted many hours or even several days and nights. 

If, in the course of a " delayed stroke," the breathing, until 
now quiet and regular, suddenly gives place to a rapid, irregu- 
lar, stertorous respiration, and if at the same time the partial 
unconsciousness deepens into a profound coma, the reflexes 
become lost, and tetanic convulsions of the whole body and 
hemicontracture of the paralyzed side make their appearance, 
then we can assume that the haemorrhage has burst through 
into a ventricle, and give an absolutely unfavorable prognosis, 
because in a few hours, more rarely in one or two days, death 
almost invariably follows. The haemorrhage itself in such 
cases is, as can be demonstrated at the autopsy, generally by 
no means copious, but the fact that it is also found, even if the 
ependyma of the ventricles be thickened and hardened, speaks 
most clearly for the high arterial pressure under which the 
blood escapes (Wernicke). The bursting of the blood into the 



APOPLECTIC EQUIVALENTS. 



223 



fourth ventricle is the most rapidly fatal, and it is in these cases 
that we sometimes observe nystagmus. 

The disturbance of consciousness in its many gradations, 
from the light vertigo to the deep coma, is the most character- 
istic, or at least the most important, symptom of an apoplectic 
attack produced by haemorrhage, and it ought not to be under- 
rated, even if it does not become fully developed, but only 
amounts to a transient slight speech disturbance, accompanied 
by a feeling of faintness and weakness. There are patients in 
whom such slight disturbances occur several times before the 
onset of a real attack. Such patients complain of transient 
vertigo, slight weakness, and heaviness in one or the other 
hand or foot ; they can at times not find the right word, the 
correct expression, or lose speech entirely for a short while. 
All these indications are premonitions, not direct forerunners 
of the attack, but symptoms which warn us, indicating to us 
that the brain is subject to alterations in the blood-pressure, a 
condition which may lead to serious consequences if the arte- 
rial walls are diseased (" apoplectic equivalents "). 

Complete absence of all disturbance of consciousness is a 
rare exception, and can only be found when the blood escapes 
quite slowly, so that the increased pressure rises only very 
gradually, and to no great degree. The patient then is seized 
with a sudden weakness, purely physical ; he sinks into a chair, 
and after a few moments, during which time there is not the 
slightest disturbance of consciousness, he becomes aware of a 
sort of difficulty in moving the extremities of one side, which, 
in the most unfavorable instances, in a short time passes into a 
genuine paralysis of that side (focal symptoms without stroke). 
Here may also be mentioned the cases observed by Romberg, 
Graves, Andral, Senator, and others, in which after a hemi- 
plegia no trace of haemorrhage was found at the autopsy, but 
only a diffuse hyperaemia of the brain could be demonstrated — ■ 
" pseudo-apoplexy." 

On the other hand, it is not a very unusual occurrence that 
a patient awakening in the morning after a quiet night's rest 
finds himself paralyzed on one side ; in such cases we are, of 
course, not able to decide how much his consciousness would 
have been impaired had he been awake. 

In every hemiplegia that occurs in the course and as a con- 
sequence of cerebral haemorrhage there is a possibility of re- 



22 4 



DISEASES OF THE BRAIN PROPER. 



generation to a greater or less extent, but whether this regen- 
eration will take place, and when, and, moreover, whether it 
will be complete or not, are questions that can not at once be 
decided. They all depend on the condition of the cortico-mus- 
cular tract, as we have pointed Out before— upon whether this 
be actually interrupted, whether its fibres in places, for instance 
at the internal capsule, be completely destroyed, or whether 
their function be only temporarily impaired in consequence of 
the increased blood pressure, so that after the cessation of the 
haemorrhage a restitutio in integrum of the nerve tissue can 
follow. In the latter case, the paralysis disappears after a few 
hours or days, while after an actual interruption of the cortico- 
muscular tract the hemiplegia is incurable, and the patient is 
deprived of the free use of the affected limbs, and, even though 
he may regain after a long time some power of motion, his 
movements will always remain awkward and restricted. 

Sometimes, and this is not very rare, a patient may have 
an apoplectic stroke after which the paralysis disappears 
quickly and entirely, but which is in a few days, on some 
slight provocation, followed by a second attack, accompanied 
by a severe permanent hemiplegia, which under certain cir- 
cumstances can cause death. Such a possibility should always 
be thought of, and we would here say that the prognosis, no 
matter how slight and favorable the apoplexy may seem, 
should always be very guarded. 

Among the " concomitant symptoms " which only excep- 
tionally persist for any length of time, and ought therefore to 
be regarded as indirect focal symptoms, may be mentioned a 
peculiar deviation of the eyes and the head — the "deviation con- 
jugue'e " of Prevost — generally toward the side of the lesion, so 
that the eyes " look toward the disease-focus." This has been 
thought to be associated with a lesion in the upper parietal 
lobule. Prevost and Landouzy gave this rule : " Le malade 
regarde son hemisphere alt ere s'il y a paralysie — il regarde ses 
membres convulses s'il y a excitation " (the patient looks to- 
ward the damaged hemisphere if he have a paralysis, if there 
be irritation he looks toward the convulsed limbs). This is 
seen, for instance, in the so-called cortical epilepsy, which we 
have spoken of on page 185. The head seems forcibly turned 
to one side, and the eyes are turned so far over to the canthus 
that we are scarcely able to test the condition of the pupil ; 
along with this symptom there is found almost always a more 



THE CEREBRAL HEMIPLEGIA. 



225 



or less marked dullness of the sensorium. Why this condition 
is generally transient is explained by the fact that the muscles 
of the eyes and neck can be innervated from both hemispheres, 
so that even if one side becomes incapable of working, the 
other can act vicariously for it. Only in bilateral haemor- 
rhages which produce a permanent paralysis of the eye mus- 
cles is conjugate deviation found to persist (cf. page 48). 

Unilateral oculo-motor paralysis on the side of the hemi- 
plegia is very rare ; it is supposed to be associated with lesions 
of the lower parietal lobule. 

After a severe attack there may be a transient polyuria 
lasting for one or two days ; the specific gravity of the urine, 
which is then faintly acid, may be 1.003 or 1-002 ; at times, but 
not always, albumen or a trace of sugar can be demonstrated. 
This some authors, among them Ollivier, were inclined to at- 
tribute to an action on the centres situated in the floor of the 
fourth ventricle, the existence of which Claude Bernard had 
already demonstrated. This polyuria after an apoplexy does 
not persist, while this may be the case in tumors of the poste- 
rior fossa, in focal lesions of the pons or the medulla oblongata, 
where it has to be looked upon as a focal symptom (Kahler, 
Zeitschr. f. Heilk., vii, 2, 3, 1886). 

In proceeding to the examination of a fresh hemiplegia — 
that is to say, one of a few days' or a week's duration — the 
following points must be borne in mind : 

The facial and the hypoglossal nerve deserve the most at- 
tention. The former is injured in its central course, and shows 
a paralysis or only a paresis in its lower branches, while the 
upper ones are intact ; the patient is unable to inflate the para- 
lyzed cheek, and can not whistle, while wrinkling of the fore- 
head on the paralyzed side presents no difficulty. Careful ex- 
amination shows distinctly that the disturbance on the para- 
lyzed side of the face is much more marked on attempting vol- 
untary movements of one side alone, whereas those of expres- 
sion — for instance, laughing, crying — are at least passably exe- 
cuted. This, again, may be explained by the fact that muscles 
used involuntarily are innervated from both hemispheres. The 
duration of the facial paralysis varies ; sometimes the difference 
between the two sides of the face disappears almost completely 
in a few days, while in other instances it may be noticeable 
for weeks or, in rare exceptions, even during the whole life. 
In this point it resembles the speech disturbance caused by a 
15 



22 6 DISEASES OF THE BRAIN PROPER. 

lesion of the hypoglossus, a disturbance which essentially con- 
sists in faulty articulation, which is noticed by the patient 
more than those who converse with him. It may disappear in 
a few hours, but may persist for months, even years, when im- 
provement in the affected side has gone on for a long while, 
and gratifying progress has already been made. A paralysis of 
the same nerve, or rather of the genioglossus muscle supplied 
by it, is also responsible if the patient is unable to protrude the 
tongue straight ; it is deviated to the paralyzed side because 
the well genioglossus is stronger than the diseased one, and 
consequently pushes the tongue over toward the side of the 
latter. 

The condition of the soft palate is not the same in all cases. 
The velum may be considerably lower on the paralyzed than on 
the well side, but it may also occupy its normal position. The 
uvula is at times deviated to the well, at times to the para- 
lyzed side, and again at other times its position may be un- 
changed. These changes do not give rise to any noticeable 
disturbance of function. 

Examination of sensibility in the first few days reveals de- 
cided alterations. Sensibility to pain in most cases is dulled 
and sensibility to touch and pressure is decreased, though to a 
less marked degree. The patient feels a pin prick either not 
at all on the affected side or, at any rate, with less acuteness. 

Of the nerves of special sense, it is especially the optic 
which takes part in the disturbance. The apoplectic attack 
may be followed under certain circumstances by hemianopia 
of the corresponding side (Gowers), often, too, by amblyopia. 

Smell and taste, as a rule, do not suffer to any great extent ; 
but there is a decrease in hearing power, so that the patient is 
no longer able to understand words spoken in an ordinary tone 
at a distance of fifteen or twenty feet. Such a decrease is not 
rare, yet an absolute (unilateral) deafness never seems to follow 
as a result of an apoplectic attack. 

With regard to mobility, examination shows that either the 
extremities of one side of the body are completely paralyzed 
(hemiplegia) or that they are impaired in the power of move- 
ment (hemiparesis). In the latter case the arm is usually more 
affected than the leg and the hand more than the arm. Indeed, 
the movements in the shoulders and elbow joint may be as 
good as normal, while those of the fingers are very awkward ; 
in such cases the leg can generally be moved quite well. The 



THE CEREBRAL HEMIPLEGIA. 



227 



muscles of mastication and those of respiration are, for the 
reasons above mentioned, almost intact, the muscles of the 
trunk are only slightly implicated, and, if at all, the change is 
only apparent in the trapezius, so that the shoulder of the 
affected side is raised less energetically than its fellow. 

The tendon and skin reflexes are, in the first few days after 
the attack, decreased or even lost on the affected side, a condi- 
tion which, as we shall see shortly, soon becomes materially 
changed. 

The sensorium usually clears up in from one to four days, 
especially in light cases. The patient again becomes conscious 
of his surroundings and recollects quite well all incidents which 
happened nearly up to the time of the attack. Thence on, there 
is, of course, a blank in his mind. On awakening, at first he 
has no idea of what has happened to him. His frame of mind 
varies according to the degree of his bodily helplessness, but, 
as a rule, is better than we might expect, considering the 
damage which has been done. Sleep is for weeks much inter- 
fered with. The patients are extremely restless ; they throw 
themselves about in bed, and are unable to remain in one posi- 
tion for any length of time. 

The further course depends upon whether the hemiplegia 
proves to be an indirect or a direct focal symptom. 

The slighter cases of indirect hemiplegia, when they have 
not completely passed off after several weeks, are at any rate 
generally improved. The one-sidedness of the face, seen at 
the beginning, has disappeared ; the tongue now is protruded 
straight, speech is again normal, the leg can be moved almost 
as freely as ever, and the only thing which is left as a reminder 
of the dangers through which the patient has passed is a certain 
awkwardness in the movements of the affected hand. 

The graver cases of indirect hemiplegia need from two to 
three months for complete recovery. For weeks after the at- 
tack the patient presents marked disturbances in motion as 
well as sensation, and only painfully and with the help of a 
stick can he hobble about his room, while the arm and hand 
are almost useless. Yet a constant progressive improvement 
of the paralyzed limbs enables us to recognize the favorable 
tendency of the case and to predict with certainty a complete 
recovery. 

In cases of direct hemiplegia also the course r of the disease 
may assume many varieties. All are characterized by the per- 



228 DISEASES OF THE BRAIN PROPER. 

sistence of the focal symptoms. The attack, too, we should 
keep in mind, need not be particularly severe nor need the 
initial general symptoms have been especially grave ; only the 
conjugate deviation of the eyes and head is a symptom which 
preferably occurs in grave hemiplegia. Its presence, therefore, 
permits a priori of an unfavorable prognosis with regard to 
complete recovery. 

In the first three or four weeks, things remain apparently 
about the same ; the paralyzed side is flaccid and about five 
ninths to one degree centigrade warmer than its fellow, the 
slightest motion is impossible, speech remains impaired, and 
the face is one-sided. It is not until from three to six months 
have passed that we are able to notice a slight improvement in 
the power of motion, so that the patient (who is still confined 
to bed) is able to move with ease some of his toes, perhaps also 
the lower leg, while in the thigh motion is still incomplete, and 
in the arm and hand quite impossible. In such cases all the 
improvement that can be expected is but small and the damage 
which the stroke leaves very apparent. After from six to 
twelve months the patient again begins to be able to use the 
paralyzed leg, which in the mean time, in consequence of the 
flaccid condition of the ankle, has become longer. The walk 
is then very characteristic. Flexion in the hip being insuffi- 
cient, the leg is brought forward by the aid of the pelvis, so 
that the affected leg trailing along the ground describes a half- 
circle around the sound one. The centre of gravity of the 
body then is transferred to the paretic leg, the knee-joint pas- 
sively extended, and the leg thus used as a stilt (Wernicke). 
If improvement goes on, the movement of circumduction grad- 
ually disappears and the paretic leg is simply dragged behind. 
The gait is so characteristic that the diagnosis, especially when 
simultaneously there is a paretic condition of the upper ex- 
tremity, can be made at a glance. 

The upper arm is slightly abducted, the forearm flexed, the 
hand hangs down, the fingers, which are fixed in a somewhat 
flexed position, are completely useless, and the patient is un- 
able to grasp large or small objects. The arm can hardly be 
raised at all, and the movements of the forearm on the upper 
arm are very limited. In the lower leg extensor are more fre- 
quently developed than flexor contractures, and it is remark- 
able that in the morning, when the patient awakens after a 
long sleep, how slight they are and how little they trouble 



THE CEREBRAL HEMIPLEGIA. 



229 



him, whereas in the course of the day they are materially in- 
creased. 

Contractures, which are in old hemiplegias hardly ever ab- 
sent, are most likely to be attributed to a shortening of the 
muscles produced by disuse. This idea is supported by the 
fact that by systematic passive exercise, begun as soon as pos- 
sible, we are able to prevent contractures ; and, if they exist, a 
proper galvanic treatment, which takes the place of passive 
motion, perceptibly diminishes them. It is true it remains 
unexplained why contractures are not found in all cases, and 
why in some the paralyzed extremities remain for life flaccid. 
That anatomical changes, too, especially, as Charcot assumes, 
the secondary degeneration of the pyramidal tract, are not 
without influence, and that, at any rate, the contractures are 
more marked the farther this secondary degeneration advances, 
can not be denied. 

A symptom which accompanies contractures, but which 
often occurs much earlier, is an increase in the tendon reflexes 
on the paralyzed side. Tapping of the triceps and biceps 
tendon of the arm, of the patellar tendon, and the tendo 
Achillis evokes lively muscular contractions. From the last 
named — the tendo Achillis — we can also obtain the so-called 
ankle clonus, of which phenomenon we shall speak later. Even 
tapping of bones is attended by jerkings, which are best seen 
in the leg when the tibia is struck (" periosteal reflex "). Here 
again we must leave the question open whether this increase in 
the reflexes is due to the degeneration in the pyramidal tracts or 
merely connected with the suspension of certain reflex-inhibit- 
ing influences in the brain. In favor of the latter hypothesis 
speaks the fact that this increase in the reflexes is occasionally 
observed as early as a few days after the stroke, at a time when 
there can be no question of degeneration in the spinal cord. 

With the skin reflexes it is just the reverse ; they are usual- 
ly entirely lost on the paralyzed side or are at least decidedly 
diminished. This is especially the case for the abdominal and 
cremasteric reflexes, which can only in exceptional cases be 
obtained on the affected side. 

Sensation either returns soon after the initial disturbance or 
is lost forever. In the latter case — i. e., where besides the 
hemiplegia there exists also a hemiansesthesia — the lesion is to 
be located in the posterior portion of the posterior limb of the 
internal capsule. The hemiansesthesia takes in, in pronounced 



230 



DISEASES OF THE BRAIN PROPER. 



cases, the whole half of the body, including the mucous mem- 
branes, and extends as far as the median line. Face and trunk 
are equally affected ; occasionally we may find that the tri- 
geminus remains exempt. 

In slight cases the disturbance is confined to the extremities 
and concerns more the sensibility to touch than the sensibility 
to pain. The patient feels the prick of a pin, but is unable to 
direct his fingers properly if the eyes are closed ; he makes 
mistakes in recognizing objects which are given him to feel ; 
he is unable to fasten small buttons, etc. Changes in the mus- 
cular sense also may exist for a considerable time, the patient 
being unable with his eyes closed to give any information 
about the position into which his hand has been brought. 

In examining sensation in hemiplegics, Oppenheim (cf. lit.) 
has noticed that at times bilateral impressions are appreciated 
only on one side ; that, for instance, if a patient is pricked simul- 
taneously in the right and left thigh, he only perceives one 
prick — namely, that on the well side, although he is perfectly 
conscious of a prick on the paralyzed side alone. 

One of the rarest of sensory disturbances is the persist- 
ent hypersesthesia of the paralyzed side, described by M. H. 
Fischer (Arch, de phys. norm, et path., February 15, 1887, ix, 
page 185). 

The psychical condition is not always the same. In certain 
cases the patients seem to have regained all their former facul- 
ties satisfactorily, so that a careful examination brings to light 
nothing more than a slight loss of will power and of the capa- 
city for grasping ideas ; but in other instances the patient be- 
comes mentally weaker and at the same time irritable. He is 
easily made to cry and is liable to sudden changes of temper. 
Such patients are, however, notwithstanding their apparent 
obstinacy, very manageable and easily guided. Again there 
are cases in which the psychical weakness becomes very ap- 
parent. The patient forgets the commonest things, the num- 
ber and the names of his children, confuses things and places, 
does not know what day of the week and what season of the 
year it is, etc. ; at the same time he may have different de- 
lusions and hallucinations. Some cases finally go on to com- 
plete dementia, which takes a course not unlike that of general 
paralysis. Legrand du Saulle has published an interesting 
study of such disturbances among the apoplectics of the Salp6- 
triere (Gaz. des hdp., 68-71, 1881). 



THE CEREBRAL HEMIPLEGIA. 



2 3 I 



In the further course of severe hemiplegias where regen- 
eration is impossible to any great extent, motor disturbances 
which we have designated as posthemiplegic (cf. lit. under 
treatise of Greidenberg) may follow. One of these is the so- 
called hemichorea, consisting of involuntary irregular move- 
ments in the paralyzed limbs, which become aggravated by 
every mental emotion and voluntary movement and which en- 
tirely cease during sleep. These movements, which are best 
studied on the upper extremity, occur more frequently after 
cerebral infantile hemiplegia than in any other affection. The 
" hemiataxia " described by Grasset (cf. lit.) is closely related 
to hemichorea, and ought to be regarded as a variety of it. 
According to Charcot, the seat of the lesion in these cases is in 
the posterior portion of the internal capsule, the posterior part 
of the optic thalamus, and in the foot of the corona radiata. 
The so-called hemiathetosis will be considered in the chapter 
on the cerebral palsies of children. 

A second class of motor disorders is made up of those pe- 
culiar involuntary movements which have been described as 
" associated movements." They are observed in the paralyzed 
extremity when the patient moves the corresponding, unaf- 
fected, one ; thus, for instance, if a patient uses his right, well, 
arm, the paralyzed arm makes similar movements, of course 
being restricted to a lesser or greater extent by any contract- 
ures which may be present. These movements have nothing 
in common with the so-called reflex movements which are 
found to occur in the paralyzed limb on stimulation of the 
sound one by the prick of a pin, the faradic current, etc. A 
peculiar instance of " associated movements " in an old hemi- 
plegia I had the opportunity of observing for months. It was 
as follows : Every time the patient yawned the left arm was 
raised involuntarily at the shoulder-joint, and was kept up 
while the yawning continued ; as soon as it ceased the arm 
dropped down helplessly. Sometimes one sees the sound 
limbs make involuntary movements if the patient attempts to 
use the affected ones, and again and again I have seen patients, 
straining to bend the paralyzed leg, become greatly astonished 
at the flexion which took place in the well leg without any 
such intention on their part. That in intended movements of 
certain muscle groups the antagonists begin to make involun- 
tary movements — that, for instance, if an extension of the flexed 
fingers be attempted, the flexion at first becomes more forcible 



232 



DISEASES OF THE BRAIN PROPER. 



before extension begins (Hitzig) — is, according to our experi- 
ence, very exceptional. 

There are other associated movements which occur in the 
paralyzed half of the face when the sound side is moved ; so, 
for instance, in laughing, the muscles of the paralyzed side are 
seen to contract equally, or even more strongly, than those of 
the well side. The origin of this phenomenon, and of the 
movements before mentioned, must be regarded as being per- 
fectly different. 

Various theories have been proposed to explain associated 
movements (Westphal, Benedikt, Broadbent, and Ross), but 
none of them can be taken as entirely explaining the facts. It 
is by no means impossible that all such motor disturbances are 
reflex in nature (Charcot and Brissaud). 

As a third posthemiplegic phenomenon we have the tremor. 
It is not rare, and that form especially which occurs on volun- 
tary movements of the affected side is rather frequently met 
with ; on the other hand, we shall very rarely have the oppor- 
tunity of observing this tremor while the extremities are at 
perfect rest. Relatively, the largest number of cases who 
presented tremor, in my experience, showed sensory changes, 
which consisted of paroxysms of pain in the affected extremi- 
ties. On a cursory examination this tremor may be mistaken 
for unilateral paralysis agitans (hemiparalysis agitans), espe- 
cially as the number of oscillations is about the same in both 
affections, 4 3 / 4 to 5 : / 4 in a second. Pronounced intentional 
tremor, which we look upon as a pathognomonic symptom in 
multiple sclerosis, I never have observed in hemiplegia. Prob- 
ably the cause of this posthemiplegic tremor has to be sought 
in the general increase of reflex activity, which, as we may 
remark here by the way, is observed besides only in a very 
few cases of tremor of a different nature. Here it seems to 
play the most important role. 

Of great interest, as well as, at times, of no small practical 
importance, is the fact that in cases of incurable hemiplegia 
the non-paralyzed side, that is, the apparently well extremities, 
undergo certain changes which we are compelled to regard 
as pathological. Thus, Pitres (cf. lit.) has found that the well 
arm loses somewhat in strength, and that this is often more 
marked in the beginning of the hemiplegia than later on. On 
an average the loss amounted to about 38 or 40 per cent, while 
no increase in the tendon reflexes could be demonstrated at 



THE CEREBRAL HEMIPLEGIA. 233 

the same time. The well leg becomes weaker, and indeed in a 
more marked degree than the arm, the strength being reduced 
in some cases even by one half. The patient, though able to 
move that leg with perfect ease while in bed, finds it almost 
useless to attempt to stand or walk. Pitres was also the first 
to notice that the patellar reflex of the sound side, as well, is 
abnormally active, an observation which is daily confirmed. 
The presence of the foot phenomenon (ankle clonus) is noted 
by Westphal and Dejerine. All authors, however (Hallopeau, 
Brissaud, Fere), agree that it is extremely unusual to find the 
later contractures on the non-paralyzed side. On the whole, 
these changes, which occur on the so-called unaffected side, 
are more marked and of greater significance to the patient 
than we should be led to suppose from a superficial examina- 
tion. 

Trophic vaso-motor changes are not uncommon in the par- 
alyzed limbs. While in the beginning of a hemiplegia the 
skin of the affected side is warmer and redder than that of the 
well side, it becomes cooler as the disease progresses, and fre- 
quently assumes a somewhat cyanotic color. The oedema 
often seen in the affected extremities is due to the absence of 
muscular movement and the consequent slowing of the blood 
and lymph current. In a patient who, two years before, had a 
pretty severe apoplectic attack with persistent speech disturb- 
ance, I have repeatedly observed slight repetitions of the 
haemorrhage, during which the speech, which had consider- 
ably improved, again became entirely unintelligible. Simul- 
taneously there was developed on each such occasion over the 
whole body, and not merely over the paralyzed right side, an 
urticarial rash which persisted as long as the cerebral symp- 
toms lasted. No doubt this was due to a disturbance in the 
vaso-motor innervation of the vessels of the skin, which reap- 
peared with the transient increase in the intracranial pressure. 
Charcot describes an acute malignant bed-sore which appears 
two or three days after the onset of the hemiplegia in the 
gluteal region, beginning as a red spot and developing in a few 
days into a brown, dry eschar six to seven centimetres broad. 
It always ends fatally, and is, according to Charcot, a purely 
trophic disturbance, an alteration in the tissue, which we can 
only attribute to nervous influences. 

The nutrition of the muscles which for years have been par- 
alyzed usually suffers but little. We can easily understand 



234 



DISEASES OF THE BRAIN PROPER. 



that a slight degree of atrophy, due to inactivity, occasionally 
manifests itself, yet the exxitability to both electrical currents 
remains normal. Only in exceptional cases is there pronounced 
muscular atrophy in the affected limbs when these, although 
their motion is impaired, can still be used to a certain extent. 
In such cases the atrophy can not be referred to inactivity, but 
we must rather assume a lesion in the trophic centres of the 
cortex, the seat of which is, however, still unknown. 

The simultaneous appearance of a haemorrhage in each 
hemisphere is exceptional. It needs hardly to be stated that 
such an accident must necessarily give rise to the gravest 
symptoms : bilateral hemiplegia — that is, paralysis of all four 
extremities — bilateral facial and hypoglossal paralysis, amauro- 
sis, and total anaesthesia. 

Diagnosis. — The diagnosis of cerebral haemorrhage may 
give rise to considerable difficulties. It is only then easy if a 
suddenly or gradually developing unconsciousness is followed 
by a paralysis or paresis of one side in a patient not suffering 
from any valvular disease of the heart. Under such circum- 
stances the case is absolutely clear, and even the most cautious 
diagnostician, if he can exclude hysteria, may safely assume a 
cerebral haemorrhage with consequent hemiplegia. 

It is a different matter where we have to make a diagnosis 
at a time when we are unable to ascertain the presence or 
extent of the paralysis, but where we are restricted to an in- 
terpretation of the unconsciousness of the patient. Under 
these circumstances we have to be familiar with the conditions 
which, besides cerebral haemorrhage, are capable of giving rise 
to unconsciousness, and be acquainted with the characteristic 
manifestations which each offers. 

In the first place we may have to deal with a simple faint- 
ing fit. The concomitant symptoms — the wax-like pallor of 
the face, the small, frequent pulse, the cold sweat which covers 
face and body — are not likely to allow us to mistake the con- 
dition for one of apoplexy, especially as the gravest symptom 
— the loss of consciousness — as a rule, is not of long duration, 
but vanishes rapidly if the patient is laid down with the head 
low, the face sprinkled with cold water, or if ammonia or eau 
de Cologne, etc., be held to the nose. The success or non- 
success of these measures will help us to settle the differential 
diagnosis in a few minutes. 



DIAGNOSIS OF CEREBRAL HEMORRHAGE. 



235 



Secondly, we may have before us an epileptiform attack 
without convulsions or the coma which so often follows epilep- 
tic fits. Here the loss of consciousness is also complete, and 
the diagnosis can only be made if we can obtain a history of 
previous epileptic convulsions, or if we are able to assume this 
from scars on the tongue. In the absence of such evidence 
the color of the face may sometimes be of value to us ; in some 
epileptics this is very pale, in cerebral haemorrhage of a pur- 
plish color, yet this rule by no means always holds good, and 
should therefore be accepted cum grano salts. 

The unconsciousness so often occurring in the course of 
a meningitis may be recognized from the temperature and the 
pulse, the peculiar drawing in of the abdomen (scaphoid abdo- 
men), the jactitations, the rigidity of the neck, and possibly 
from the existence of a papillitis. 

In the beginning and in the course of the progressive paral- 
ysis of the insane (dementia paralytica) apoplectiform attacks 
occur which resemble those produced by cerebral haemorrhage 
very closely indeed, and which only can be recognized as be- 
longing to the former disease from the previous history of the 
patient (and later from the results of the autopsy). If we can 
get no inforrhation about the history the differential diagnosis 
is impossible. 

Intoxication with chloroform and alcohol may be attended 
by complete loss of consciousness. An individual in the uncon- 
sciousness of alcoholic intoxication is just as hard to arouse as 
one in apoplectic or epileptic coma, and the diagnosis may pre- 
sent some difficulties under certain circumstances — when, for 
instance, nothing can be learned about the cause, or what has 
immediately preceded the loss of consciousness. Usually, how- 
ever, it is easy enough. Sometimes the smell of the ingested 
substance puts us on the right track, sometimes prompt reac- 
tion to energetic stimuli applied to the skin may make our 
diagnosis clear. As long as we are not sure of our ground, we 
ought to abstain from all therapeutic measures. Of opium or 
of morphine poisoning we need only think when the pupils of 
the patient are conspicuously small. A degree of myosis as 
high as we find in opium poisoning has only its parallel, and 
then but rarely, in haemorrhages into the pons, which are 
rapidly fatal. 

Uraemic coma can easily be excluded, if we are able to ex- 
amine the urine, and can detect neither albumen nor tube casts ; 



236 DISEASES OF THE BRAIN PROPER. 

besides this, with the history, the examination of the heart for 
a possible hypertrophy should not be forgotten. 

Diabetic coma, finally, is characterized by a peculiar fruity 
odor which comes from the mouth of the patient. It, of 
course, only enters into the question if sugar can be demon- 
strated (or has previously been repeatedly detected) in the 
urine. 

The anatomical nature of the hemiplegia may remain en- 
tirely obscure, and only in certain cases are we able to give a 
decided opinion about it. 

Whether hemiplegia following a stroke is due to haemor- 
rhage or embolism can only be determined by accompanying 
circumstances. The existence of valvular lesions and of athe- 
roma speaks for embolism ; nephritis, heart hypertrophy, albu- 
minuria for haemorrhage ; yet this rule has many exceptions, 
and we may assume that in about half the cases a correct diag- 
nosis is impossible. 

The meningitic hemiplegia has these points in common 
with the hemorrhagic — namely, the paralysis on one side and 
the " conjugate deviation " ; but, as we have before pointed out, 
in meningitis we generally have the characteristic rigidity of 
the neck and the scaphoid abdomen ; where these latter symp- 
toms are not even suggested, a differential diagnosis, or rather 
the recognition of a hemiplegia as of meningitic origin, is im- 
possible. 

The hysterical hemiplegia, finally, if it persist for a long 
time, and if other hysterical symptoms, as anaesthesias or con- 
tractures, are wanting, can never with any certaintv be differen- 
tiated from that depending upon cerebral haemorrhage. Both 
may present the same peculiarities, and a decision as to which 
condition we are dealing with may be beyond the powers even 
of the practiced diagnostician. We are indebted to Charcot 
for a new symptom, to which he has drawn attention, and 
which is said to be characteristic of hysterical hemiplegia — 
namely, a paroxysmal spasm of the muscles of the cheek of one 
side, associated with an excessive deviation of the tongue to 
the same side. This " glosso-labial hemispasm " never exists in 
organic lesions of the pyramidal tract, and is therefore pathog- 
nomonic for hysterical hemiplegia (Brissaud and Marie, cf. lit.). 

If the question of the anatomical seat of the haemorrhage is 
to be considered in our diagnosis, we must in the first place 
not forget that the mere existence of a hemiplegia is not suf- 



PROGNOSIS IN CEREBRAL HEMORRHAGE. 



237 



ficient to give us an answer, for as long as we do not know 
whether to regard it as a direct or an indirect symptom, we 
can say nothing positive. If we further add that even an indi- 
rect hemiplegia may persist for years, we can easily see with 
what difficulties we meet in attempting a topical diagnosis. It 
may be quite true that in a great many cases where an apo- 
plectic attack is followed by hemiplegia, the lesion is situated 
in the internal capsule, and we have become accustomed to as- 
sociate in our minds a certain typical clinical picture — that is, 
hemiplegia with more or less marked sensory changes — with a 
lesion in the internal capsule. We must, however, in making a 
diagnosis of that kind always keep in mind that an indirect 
hemiplegia may be produced by lesions in any part of the 
brain, by lesions in the frontal, in the parietal, the occipital 
lobe, of the thalamus, of the lenticular nucleus, of the external 
capsule, and that, as we have also said, the duration of such in- 
direct hemiplegias is by no means always restricted to a period 
either of a few days or a few weeks, Hence a certain reserva- 
tion must ever be observed by a prudent diagnostician, and he 
should only then speak with some certainty if he has some 
other direct focal symptom to guide him. Among these, we 
have, for instance, sensory aphasia for the (left) temporal lobe ; 
for the occipital lobe, hemianopia ; for the optic thalamus (with 
a high degree of probability), posthemiplegic chorea ; for the 
crura, alternating oculo-motor paralysis ; for the pons, alternat- 
ing facial paralysis. 

Prognosis. — After all that has been said, we hardly need to 
add anything about the prognosis. Any cerebral haemorrhage 
is a grave event, which puts the life of the patient in danger, or 
rather it is a symptom which denotes that a grave arterial dis- 
ease, without which a haemorrhage never occurs, has reached 
a state dangerous to life. If once a haemorrhage has occurred 
we are not sure but that it may be repeated at any moment, 
since the condition which favored it, the brittleness of the ar- 
terial walls, means a lasting incurable predisposition to a fresh 
haemorrhage. 

In the presence of a recent apoplectic attack, it is impossi- 
ble for us to give a certain prognosis, or to predict what will 
follow. The severity of the disturbance of consciousness is in 
a way indicative, and we may say that the severer this is 
found to be — in other words, the greater the traumatic effect of 
the haemorrhage — the less favorable is, cceterus paribus, the out- 



2 3 8 



DISEASES OF THE BRAIN PROPER. 



look with regard to life, as well as with regard to recovery. 
Yet exceptions occur, and even a very severe coma which 
has persisted for hours does not only not always produce 
death, but need not necessarily leave behind it focal symptoms, 
as hemiplegia or the like, and such patients may then be well 
for years afterwards. Unfortunately, so favorable a result is 
rarely met with. As a rule, a haemorrhage of any considerable 
size is either fatal or is followed by a hemiplegia. 

As to the difference in the prognosis for the individual, in- 
direct as well as direct, focal symptoms, most that deserves 
mention has already been spoken of. The indirect symptoms, 
as a rule, disappear after a certain time, and a restitutio in in- 
tegrum is not impossible ; the direct ones are only curable 
when vicarious innervation takes place from the unaffected 
hemisphere which assumes the function of the damaged one. 
This can be the case, for instance, in unilateral facial and hypo- 
glossal paralysis, and in the lateral deviation of the eyes (lesions 
of the lower parietal lobule, cf. page 173); it may also occur in 
motor aphasia if the patient is still capable of learning to speak 
with his right hemisphere (lesion of the region of Broca, page 
175). On the other hand, it does not occur in cases of direct 
hemiplegia due to a lesion of the internal capsule ; then the 
paralysis is incurable, and the improvement which may take 
place is always very imperfect, although a properly conducted 
treatment may effect some amelioration, and thus conduce 
much to the well-being of the patient. 

Treatment. — The primary affection, the disease of the ar- 
teries to which cerebral haemorrhage is due, is beyond the 
reach of therapeutics. We possess no remedy which can 
cause the miliary aneurisms to disappear, and our efforts are 
confined to combating those symptoms which accompany, and 
those which follow the haemorrhage. Thus we have to deal 
with (1) the apoplectic attack itself ; (2) the anatomical changes 
which are produced in the brain by the haemorrhage ; (3) the 
focal symptoms, the paralysis (or paresis) cf one side ; and, in 
general, all motor and sensory disturbances referable to the 
attack. 

(a) The treatment of the attack itself varies according as we 
have to deal with a suddenly or gradually developing apo- 
plexy. In the former case we may assume that the haemor- 
rhage has already stopped when we first see the patient, 
whereas in the second case the presumption that the bleeding 



TREATMENT OF CEREBRAL HEMORRHAGE. 



239 



is still going on is justifiable, and hence all measures which 
tend to arrest the haemorrhage are strenuously indicated at 
once. One of these is venesection, which produces a fall in 
the blood pressure, and should always be resorted to in cases 
where, after (or during) a haemorrhage, the carotids are found 
throbbing, the action of the heart is tumultuous, and the face 
red and congested. The success is sometimes surprising. The 
patient, who just before was comatose and motionless, with 
stertorous breathing, immediately after a free bleeding begins 
to breathe more quietly, and evidently with greater ease. He 
stirs, opens his eyes, and becomes conscious. In such a case 
venesection was the only measure indicated ; it could not have 
been replaced by anything else — in short, it has saved the pa- 
tient's life. If the pulse is small, the face pale, and the heart 
sounds are weak, no one will ever think of taking away blood. 
Then the administration of stimulants will be found useful ; of 
course, they have to be given with great caution, and be se- 
lected carefully. Vinegar enemata, sinapisms, and ether injec- 
tions may be tried. Changes in the blood pressure of the brain 
ought to be avoided most carefully ; they may be produced 
by turning the patient in bed, by shouting at him frequently, 
and by other attempts to wake him from his coma. The 
physician will have to warn the friends against doing this, and 
do his best to have the patient left quiet and undisturbed. If 
the face is congested, he will order his head to be placed high 
and have him kept in one position. Local bleeding from the 
head is, if not directly harmful, absolutely useless. If bleeding 
is indicated at all, we shall choose venesection — cupping and 
leeching are matters of so much detail and are so slow in their 
action that they can not be recommended. 

Immediately after the attack has passed off and the patient 
has regained consciousness the chief task of the physician is to 
see that he has absolute rest. Even more than any other sud- 
den illness, apoplexy produces the greatest excitement and 
consternation in a family, and it can hardly be wondered at 
that this gives place to the greatest joy when the patient, who 
has already been given up, is seen to return to life and that 
each member of the family is anxious to express his feeling of 
satisfaction. All such outbursts may be very harmful to the pa- 
tient, and these demonstrations must be crushed by the physi- 
cian with iron firmness in order to avoid any emotion on the 
part of the patient; besides, he should give directions as to a 



240 



DISEASES OF THE BRAIN PROPER. 



proper bed, which will answer all the therapeutic and hygienic 
requirements of the case, and, above all, from the very first 
due precautions against bed-sores ought to be taken. Proper 
arrangements should be made for the reception of the stools 
and the urine. The head ought to be covered with thin com- 
presses, cooled with ice water or with a light ice-bag that will 
exert no pressure. Any simple medicine which contains acids 
or cream of tartar or tartar, boraxat. and the like is sufficient 
for the first few days, during which the patient ought to be 
fed upon a light, nourishing, but unstimulating diet. 

{p) The treatment of the focal lesion in the brain — that is, 
of the place where the haemorrhage has occurred — should not 
be begun until a considerable time has elapsed after the gen- 
eral symptoms have abated. This will usually be from about 
four to six weeks after the attack. Whether it is actually 
necessary to wait so long we do not know, but, as a matter of 
fact, we are afraid to undertake any active measures at an 
earlier moment, and certainly if a physician should go contrary 
to tradition, and if accidentally another haemorrhage should 
occur, he would lay himself open to severe censure on the part 
of the family. 

On the other hand, it seems more than doubtful whether 
we are able to influence the disease-focus in any way by treat- 
ment or succeed in hastening the absorption which we desire. 
It is, however, supposed that this can be accomplished in two 
ways — namely, by internal and external remedies, by potassium 
iodide and mercury, and by galvanic treatment respectively. 
The iodide treatment is based on the supposed absorbent prop- 
erties of the drug. Whether it possesses such a power to any 
great degree is doubtful, and the fact that it so frequently fails 
to give good results seems to speak very much against it. On 
the other hand, there is no question but that iodide, if used for 
any long period of time, acts deleteriously on the stomach and 
spoils the appetite and may lead to symptoms of intoxication. 
An unprejudiced practitioner who does not administer medi- 
cines in a routine way will therefore always first ask himself 
which of the two is the lesser evil — whether he should renounce 
such help as is supposed to be derived from the remedy in the 
process of absorption and keep the patient's appetite in a good 
condition, or whether he should depend upon the more than 
doubtful action of the drug and at the same time ruin the pa- 
But if we have once decided to administer 



TREATMENT OF CEREBRAL HEMIPLEGIA. 



241 



iodide of potassium, let it be done boldly, and let 2.0, 3.0, 5.0 
(30, 45 to 75 grains) a day in one or two doses be given in hot 
milk. Given in this way the administration of the drug is less 
likely to be followed by unpleasant effects than if we order a 
tablespoonful three times a day of a solution of iodide, 4.0-8.0 ; 
water, 200 ( 3 j - 3 ij to § vj). The mercurial inunctions to the 
portion of the skull corresponding to the focus are not harmful 
if any symptoms of intoxication are watched for and salivation 
is at once treated energetically ; but their success is in no way 
greater than that obtained with potassium iodide. 

With regard to the galvanic treatment, it must, first of all, 
be absolutely admitted that it is possible to act upon the brain 
with the galvanic current. The peculiar phenomena which 
occur during galvanization of the head — vertigo, seeing of 
sparks, etc., the cerebral nature of which can not be doubted — 
speak strongly in favor of such a possibility, and the experi- 
ments of Loewenfeld on animals seem to indicate that these 
are due to an influence on the circulation in the brain. Whether, 
however, the galvanic current possesses, besides this undoubted 
action on the vaso-motor nerves, definite catalytic properties, 
and, if so, in a measure sufficient to enable us with its help to 
influence the disease-focus, nobody knows. We will suppose 
this and hope that it is so, because it is the only weapon upon 
which we have to depend. The best and most reliable electro- 
therapeutists, Erb at their head, with his unusually wide ex- 
perience, admit the scarcity of positive results from such a 
treatment, and acknowledge that in by far the greater number 
of cases they are negative (Erb, Handbuch der Electrothera- 
pie, page 320, Leipzig, 1882). Yet cases may occur where the 
physician is forced to resort to galvanization of the head — 
" the electrical treatment of the brain." He should therefore 
be familiar with the mode of application. Only large electrodes 
ought to be used. Fig. 81 represents the head electrode of 
Erb. The anode being placed on the forehead, the cathode on 
the neck, weak currents without make or break should be al- 
lowed to pass through the head of the patient for from one 
minute and a half to two minutes. Transverse and oblique 
currents may also be tried. (Details are to be found in Erb's 
text-book on electro-therapeutics, page 325). 

(c) The treatment of the hemiplegia and the posthemiplegic 
motor disturbances demands, if any success is to be expected, 
much perseverance on the part of the patient as well as of the 
16 



242 



DISEASES OF THE BRAIN PROPER. 



physician. If we can not familiarize ourselves with the idea 
that for weeks and months the same procedures and manipula- 
tions have to be gone through in exactly the same way, we 
should not begin the treatment at all nor order it to be under- 
taken. We shall then at least spare ourselves the disappoint- 
ment of a failure ; yet with patience, and where the necessary 
means are not wanting, it should be undertaken. The cases, 




Fig. 81.— The Large Head Electrode (covered with Sponge) of Erb. 

where a systematic treatment for a long time has benefited the 
patient very materially, are numerous enough, and they would 
undoubtedly be met with more frequently if a fair trial were 
given it more often than is unfortunately the case. 

From internal medicines absolutely no effect on the hemi- 
plegia is to be expected, and even the most sanguine thera- 
peutists, whose faith in drugs is unbounded, abstain here from 
fruitless attempts. The same may be said about the posthemi- 
plegic motor disturbances, and if we here make mention of the 
use of veratrine (0.002 to 0.003 [g r - : / 3 o to J / 20 ] a day in pills) 
against the posthemiplegic tremor, it is only to declare the utter 
futility of this medicament. We have here also to resort chiefly 
to electrical treatment, but with this difference, that the good 
results observed here are much more frequent and much more 
marked than in treating the disease-focus. Definite rules for 
the electrical treatment of the focal lesions as well as the hemi- 
plegic and the posthemiplegic phenomena can not be given. 
Every experienced electrotherapeutist follows certain rules 
and principles which he has found out for himself in the course 
of years from personal observation. Thus one claims only to 



TREATMENT OF CEREBRAL HEMIPLEGIA. 



243 



accomplish his end with quite weak, while the other has seen 
better results from the use of strong currents. The one uses 
galvanism, the other by preference the faradic current. Every 
one adduces reasons for his own method, which, as a rule, are 
strongly combated by other writers who claim to possess in- 
finitely more experience. 

Above all, the wishes of the patient should guide us in de- 
ciding which mode of electrization should be chosen. One 
man will have a genuine idiosyncrasy against the faradic cur- 
rent, and more especially against the faradic brush. Another 
can not stand strong galvanic currents ; they excite him, make 
him nervous, and disturb his sleep. In a very general way we 
may lay down the rule that in paralytic conditions most is 
accomplished by the galvanic current, with frequent makes 
and breaks, so as to produce contractions of the muscles. In 
conditions of irritation, especially contractures, on the other 
hand, most is accomplished by local faradization. We hardly 
need to insist that the greatest attention must be given to the 
groups of muscles most severely affected — for instance, in the 
upper extremities, to the extensors. The faradic treatment 
may, especially if contractures are threatening, be begun earlier 
than is allowed by our rule given above, even twelve to four- 
teen days after the cessation of the general symptoms, without 
any danger to the patient. 

Patients in good circumstances expect their physician to 
send them to a watering-place every year, as a stay there is a 
pleasant change from the monotonous electrical treatment, and 
we can not blame anybody for putting great faith in it. Un- 
fortunately, these hopes are not by any means justified, and 
by a course of treatment at Oeynhausen, Wildbad, Gastein, 
and Ragatz, where, by the way, the temperature of the baths 
ought not to exceed 93 F., painfully little is accomplished, cer- 
tainly a great deal less than by electrization or this alternated 
with massage. The latter ought only be carried out by well- 
trained masseurs, and only with the greatest care. From the 
cold-water treatment we also have seen little success on the 
whole, although it is decidedly to be preferred to the simple 
hot baths and the like. This also must be administered care- 
fully and must be adapted to the idiosyncrasies of the patient, 
a rule which is unfortunately not always observed. Hydro- 
therapeutics can not be learned in the clinics, where only an 
occasional remark is made about it, but deserves and demands 



244 DISEASES OF THE BRAIN PROPER. 

a practical study in establishments where this treatment is in- 
telligently and carefully conducted. The reason why it is not 
estimated everywhere as highly as it ought to be is because it 
is frequently not understood. Those who wish to acquire the 
theory of this treatment thoroughly I would refer, among 
other works, to the excellent text-book of Winternitz. 

While we have seen, then, how helpless therapeutics is 
against cerebral haemorrhage and its consequences, we have, 
on the other hand, the satisfaction of knowing that so much 
success is promised by a timely and appropriate prophylaxis, 
that we must recommend it most earnestly to all individuals of 
a so-called apoplectic habit, all who are inclined to cerebral 
congestion, all patients with a heart hypertrophy, and, finally, 
all those with hereditary tendencies. They should try to avoid 
putting on too much flesh and shun everything which would 
conduce to the production of an undue increase in the blood 
pressure. Among the most important rules upon which we 
must insist are moderation in eating, regulation of the bowels, 
frequent exercise in the open air, systematic gymnastics in- 
doors — for instance, on the " ergostat " of Dr. Gartner, of 
Vienna, a small apparatus which can easily be kept in the 
room and on which a large amount of work, measured by 
kilogramme-metres, can be done (the work can be prescribed 
in kilogramme-metres). This apparatus I can highly recom- 
mend, as I have very often seen good results from its use. To 
avoid increase in the blood pressure, the use of alcohol, coffee, 
and other stimulants, finally, all excitement, be it sexual or of 
any other kind, should be interdicted. Unfortunately, these 
warnings of the physician are not listened to until it is already 
too late, and men who will protect themselves in time and 
give up some pet habit — the customary nap after dinner or 
the like — in order to avoid a danger that only threatens, are 
few and far between. 

LITERATURE. 

Nothnagel, Handbuch der Krankheiten des Nervensystems, I, Bd. xi ; Hand- 
buch der spec. Pathologie und Therapie, von Ziemssen. Leipzig, 1878. 

Wernicke, loc. cit., ii, p. 3 et seq. 

Maeltzer. Ueber Pseudoapoplexien des Gehirns. Inaug. Dissert., Breslau, 
1 881. 

Friedlander, R. Neurol. Centralbl., ii, 11, 1883. 

Dignat, P. Progres med., xi, 39-41, 1883. 

Oppenheim. Neurol. Centralbl, 23, 1885. 



EMBOLISM OF THE CEREBRAL ARTERIES. 245 

Loewenfeld. Studien iiber Aetiologie und Pathogenese der spontanen Hirnblu- 
tungen. Wiesbaden, 1886. 

Greidenberg. Ueber die posthemiplegischen Bewegungsstorungen. Arch, fur 
Psych., xvii, 1, p. 131, 1886 (with numerous references). 

Stephan. Les tremblements prae- et posthemiplegiques et leurs rapports avec 
les affections cerebrales. Revue de med., mars 1887, p. 204. 

Hochhaus. Meningitische Hemiplegie (from Furbringer's clinic in Friedrichs- 
hain). Berl. klin. Wochenschr., 1, 1887. 

Braddon. On the Haemo-dynamics and Treatment of Cerebral Haemorrhage. 
Lancet, October 15, 1887. 

Eppinger. Pathogenesis, Histogenesis und Aetiologie der Aneurysmen. Ber- 
lin, Hirschwald, 1887. 

Loewenfeld. Zur Lehre von den Miliaraneurysmen des Gehirns. Wiener med. 
Wochenschr., No. 47, 1887. 

Brissaud & Marie. De la deviation faciale dans l'hemiplegie hysterique. Progres 
med., No. 5, 7, 1887. 

Achard. De l'apoplexie hysterique. Arch, gener., 7me ser., xix, p. 39, 
1887. 

Striimpell, loc. cit., p. 352 et seq. 

Eichhorst, loc. cit., p. 376 et seq. 

Dercum. Journ. of Nerv. and Ment. Diseases, xiv, 11, 12, 1887 (Hemiplegia 
urasmica). 

Mobius. Centralbl. fur Nervenheilk., x, 21, 1887 (hemiplegia and psychical dis- 
turbances after whooping-cough). 

Abercrombie. Brit. Med. Journ., January 14, p. 76, 1888 (fatal hemiplegia in a 
child ; autopsy). 

Gartner. Der Ergostat und seine therapeutische Anwendung. Wien, 1888. 



2. Embolism and Thrombosis of the Cerebral Arteries. 
Encephalomalacia. 

Pathological Anatomy. — We have already adverted to the 
fact that the arteries of the cortex anastomose among them- 
selves, while those of the basal ganglia are what we call ter- 
minal arteries ; from this it is evident that the embolus has 
quite a different significance where it plugs up an artery of 
the former type to that which it possesses when the ob- 
structed vessel is a terminal artery, and no collateral circula- 
tion is possible. In the first case the collateral circulation 
compensates for the damage, while in the second case we are 
bound to have a necrosis in the areas supplied by the ob- 
structed artery, a " focus of softening." It is unnecessary to 
dwell much upon the important bearing of this fact ; suffice 
it to say that the arteries usually concerned are the main 
branches and, above all, the middle cerebral. The reason 
why embolic processes are more frequent on the left than on 



246 



DISEASES OF THE BRAIN PROPER. 



the right side has already been explained (p. 213). Brain em- 
boli originate in the same manner as emboli in other organs ; 
among the causes are diseases of the left heart — chronic 
endocarditis, mitral disease, and weak heart — aortic aneur- 
isms, more rarely diseases in the pulmonary circulation. Thus 
in certain cases purulent particles may pass from the lungs 
into the pulmonary vein (in ulcerative bronchitis, gangrene of 
the lungs, etc.), and be carried into the systemic circulation. 
Polchen (cf. lit.) has also shown that certain poisons, espe- 
cially carbon monoxide, as it seems, may produce softening 
of the brain substance. According to him, the CO while 
circulating in the blood acts injuriously on the nutrition of 
the vessels, and brings about fatty degeneration and calcifica- 
tion in them. Hence there finally results a necrosis of the 
tissue. It is possible that phosphorus acts in a similar way. 
Age plays a still less important role in the aetiology of em- 
bolism than in that of haemorrhage, whereas the influence of 
sex can not be denied, as it is well known that by far more 
women are attacked by cerebral embolism than men ; it is 
possible that this is the case owing to the greater frequency 
with which we find articular rheumatism with its accompany- 
ing heart lesions in the female sex, especially in its younger 
members. The puerperal state may also have something to 
do with it. 

Thrombosis of the cerebral arteries is either produced by 
an atheromatous process which narrows the lumen of the ves- 
sel, and by slowing the blood current gives rise to coagulation, 
or by an abnormal proneness of the blood to coagulate. The 
first happens frequently in old people, and we can fairly say 
that atheroma is just as often the cause of senile softening as 
miliary aneurisms are the cause of cerebral haemorrhage. The 
abnormal tendency to coagulate (hyperinosis), which the blood 
presents in the puerperal state, in pneumonia, etc., is rarely or 
never the only cause of coagulation. It can not be said to do 
more than favor it, and hence we need not go further into the 
question. Considerable general increase in the intracranial 
pressure may give rise to thrombosis (compression thrombosis), 
as also the pressure exerted on the vessels which occurs some- 
times in basilar meningitis. If, in addition, the arterial walls are 
diseased — for instance, by tuberculosis or syphilis — the con- 
ditions are still more favorable for the formation of thrombosis. 
According to Gerhardt, the hemiplegias which occur in the 



CEREBRAL EMBOLISM. 



247 



course of basilar meningitis are due to thrombosis with second- 
ary softening. 

Finally, we should remember that traumatism — a fall or a 
blow upon the head — may produce a disease in the arteries 
which long after may give rise to thrombosis. 

The necrosis of the brain tissue which follows the cutting 
off of the arterial blood supply is called softening, encephalo- 
malacia, and we speak, according to the special ^etiological fac- 
tor, of a traumatic, an embolic or thrombotic, and an atheroma- 
tous (senile) softening. The process is as follows (Wernicke) : 
The vessels in the area from which the blood supply is cut off 
collapse, the lymph spaces dilate and through aspiration be- 
come filled with cerebro-spinal fluid, so that the whole tissue 
appears soaked, and the recent focus of softening shows a de- 
cided increase in volume ; the nerve fibres and nerve cells then 
become macerated in the fluid, and soon undergo destruction. 
With the microscope we detect varicosities of the nerve fibres, 
myelin drops, and the neuroglia and the connective tissue 
appear cedematous. If many red corpuscles are present, the 
coloring matter coming from them gives to the whole focus 
a yellowish tint ; such a discoloration is especially seen in the 
cortex {plaques jauncs, Charcot) ; the white matter which lies 
beneath is usually of a lighter tint. If then no sufficient col- 
lateral blood supply is established, which, as seems not impos- 
sible in a recent focus, might produce complete regeneration, 
there commences to develop in from thirty-six to forty-eight 
hours a fatty retrograde metamorphosis of the necrotic tissue. 
Polynuclear leucocytes emigrate from the dilated blood-vessels 
and invade the necrotic tissue ; they take up the fatty parti- 
cles, and some reach the blood current again through the 
lymph channels as compound granular corpuscles. The latter, 
which are invariably present in foci of softening more than two 
days old, on account of their infiltration with fat granules, are 
larger than the normal leucocytes. A part of them seem to 
undergo fatty degeneration, others seem to be transformed into 
myelin drops, especially in old foci. A quite gradual absorp- 
tion of the dead and disintegrated brain tissue takes place, and 
a so-called cyst is formed, which can not be distinguished from 
that following a brain haemorrhage ; more rarely we find a 
cicatrix of connective tissue, which becomes as hard as car- 
tilage, and grates under the knife. Softenings, which from the 
onset take a chronic course, have frequently been found to 



248 DISEASES OF THE BRAIN PROPER. 

form sclerotic cicatrices, so that the softening can eventually 
become a sclerosis (Wernicke). 

In softening of the cortex quite considerable areas may be- 
come deficient, which are partly replaced by serous fluid, 
partly by thickened pia. The convolutions, which sometimes 
remain, present a yellowish discoloration, appear atrophic, and 
are of a firm sclerotic consistence. 

Symptoms and Diagnosis. — Just as in haemorrhage, we 
may in embolism have symptoms which have to be regarded 
as premonitory of the regular attack. They resemble very 
closely those above described, and chiefly consist of vertigo, 
headache, an occasional feeling as of pins and needles in the 
limbs, etc. The headache may be especially prominent ; it 
may persist for weeks with undiminished intensity, and then 
disappear, or be followed by a distinct deficiency in memory 
or beginning mental decline. 

The attack proper, which occurs at the moment the lumen 
of the vessel is completely obstructed by the embolus, may 
simulate the apoplectic attack so closely that it may be abso- 
lutely impossible to distinguish the one from the other. All 
the above described differences in the nature and degree of 
disturbance of consciousness may be met with here also, and 
though it is true that at times the attack sets in with more vio- 
lent epileptiform convulsions, that the face is less congested 
and respiration less disturbed, these points are by no means 
sufficient for a differential diagnosis. It is supposed that com- 
plete loss of consciousness speaks more against embolism and 
for haemorrhage, and the early disappearance of the paralytic 
symptoms present point rather to embolism. Gerhardt con- 
siders (Berl. klin. Wochenschr., May 2 and 9, 1887) a well- 
pronounced aphasia to be in favor of embolism in doubtful 
cases. 

In embolism the attack is not evoked by an increase in the 
blood pressure, as in apoplexy, but by a " negative pressure." 
" Since the vessels lying to the peripheral side of the embolus 
suddenly collapse, and the blood contained in the capillaries 
flows into the veins owing to the vis a tergo exerted by the 
contraction of the vessels, a vacuum is suddenly formed in 
the tissue, and hence a negative blood pressure is produced " 
(Wernicke, loc. cit., p. 133). In its efforts to fill up the empty 
space, the brain parenchyma is bound to be subjected to a 
more or less considerable traction from all sides, which may 



ENCEPHALOMALACIA. 249 

sometimes lead to disintegration. If only a very small area is 
affected by the embolus, a regular attack may not take place 
and consciousness not be lost ; if it is very large, various in- 
direct symptoms may appear, and indeed even the non-affected 
hemisphere be implicated. But even after a severe stroke and 
after consciousness has been lost for quite a long time, a favor- 
able event is by no means impossible, because the tissue does 
not necessarily disintegrate, as in haemorrhage, but an equaliza- 
tion of the blood pressure can take place, which will cause the 
disappearance of all the symptoms. 

Cerebral thrombosis rarely gives rise to a stroke, owing to 
the slowness with which the process takes place, and when an 
apoplectiform attack actually does occur, it must be due to the 
previous obstruction of, other, neighboring vessels. We had 
a considerable area dependent for its blood supply on a single 
vessel which before remained open, but has now gradually 
become so narrow that the pressure in it becomes too low to 
keep up the function (Wernicke). 

The necrosis (softening, encephalomalacia) to which the ob- 
struction of an artery, if lasting sufficiently long, is bound to 
give rise, manifests itself by certain focal symptoms, which 
may, just as. in haemorrhage, be divided into direct and indi- 
rect. Among the indirect the hemiplegia, often attended with 
hemianaesthesia, which closely resembles that described above, 
is the most important. Monoplegias also and hemianopia may 
set in without a definite stroke, and may be produced indirectly 
from the focus of softening, which lies in close proximity to 
the part the functions of which are interfered with. If an em- 
bolus obstruct an artery which can communicate by anasto- 
moses with those of neighboring areas, and thus the damage 
can be compensated, we shall meet with transient focal symp- 
toms (Wernicke), which at the most require eight days for 
complete recovery. 

To determine the exact seat of the focus of softening, we 
must go to work with the same caution as in making a topical 
diagnosis of a cerebral haemorrhage. Here as there we have 
to look for direct focal symptoms, and it is to these that most 
attention should be given in our examination ; on the other 
hand, we must not forget that a focus of softening, even if it 
be of considerable extent, may pass through all its phases with- 
out a single symptom. No one region of the brain seems to be 
more exposed to softening than another. We found that the 



250 



DISEASES OF THE BRAIN PROPER. 



number of haemorrhages at the base largely preponderated over 
those in the cortex ; in embolism this is not the case. It is only 
because the surface covered by the cortex is much larger than 
that of the brain stem that we find in the latter numerically 
less cases of softening than in the cortex (Wernicke). The 
thalamus and pons are only rarely the seat of isolated soften- 
ing, while haemorrhages are found there much more frequently, 
whereas the medulla oblongata is more commonly the seat of 
softening. To diagnosticate haemorrhage in the medulla ob- 
longata during life is practically impossible, as in these cases 
death is almost instantaneous. 

Prognosis. — The prognosis in embolism is, ceteris paribus, 
in general better than that of haemorrhage. Not only is the 
outlook for complete recovery more favorable even if the 
attack has been severe and has lasted for a considerable time, 
but in most cases the danger to life is far less than in apoplexy. 

Indirect action upon the medulla oblongata, in consequence 
of which the urine may contain albumen or sugar, is a rare 
occurrence. Even a softening of considerable extent may ex- 
ist for a relatively long time without the manifestation of any 
grave general symptoms. Yet an unfavorable turn is not im- 
possible, and this should always be feared if a sudden and 
marked elevation of temperature takes place. 

Treatment. — The treatment is very limited ; indeed, embol- 
ism as such, and the necrosis produced by it, are entirely out of 
its reach. It can only be directed against the attack or consist 
of the prophylactic measures by which we may hope to prevent 
the occurrence or repetition of the accident. The latter un- 
doubtedly is the more important, and much can be accomplished 
by repeated local bleeding from the head (Laborde), a proced- 
ure which is also indicated in the treatment of the attack itself, 
as the cerebral circulation is possibly favorably influenced by 
it. That absolute rest is strongly indicated in cases where heart 
disease exists, needs hardly to be mentioned. Where there is a 
reasonable suspicion of syphilis, potassium iodide, 2.0-5.0 (grs. 
xxx-lxxv) pro die, ought to be exhibited (cf. p. 241). 

Where there are multiple foci of softening the symptoms 
naturally depend on their seat. At the autopsy a number of 
such foci may be found which could not be diagnosticated 
during life because they were too small and were situated in 
so-called indifferent places. If several portions of the brain are 



PSE UD 0-B ULBA R PARAL YSIS. 



2 5 I 



affected, each of which gives rise to a focal symptom, there may 
be a complication of the most varied clinical manifestations. 

Of great practical interest is the observation to which of 
late years attention has repeatedly been called, namely, that 
foci of softening may occur in that cerebral portion of the 
cortico-muscular tract which contains the fibres destined to 
supply the muscles used in speaking and swallowing. These 
fibres pass from the lower third of the central convolutions, 
where the supposed centres for the hypoglossus and facial are 
situated, and end in the nuclear region of the medulla ob- 
longata (cf. Fig. 75, page 209). Such foci have again and 
again been found. Sometimes they were bilateral and situ- 
ated in the basal ganglia, especially the lenticular nucleus, 
sometimes on one side only — e. g., in the right corpus striatum 
— and it has been observed that they sometimes give rise to a 
complication of symptoms which simulate most closely those 
of Duchenne's bulbar paralysis. The fact, however, should be 
especially emphasized that the occurrence of such a focus on 
one side is sufficient by itself to produce all these symptoms 
(Lepine and Kirchhoff, cf. lit.). 

The disturbances which go to make up the clinical picture 
are at times exclusively, always chiefly, referable to speech 
and deglutition. They resemble at first sight so much those 
of bulbar paralysis that the name pseudo-bulbar paralysis, or 
paralysis glosso-labio-pharyngea cerebralis, seems justifiable. 
Still, there are some points which should help us to avoid mis- 
takes. Thus, while the beginning of the true bulbar paralysis 
is slow and gradual, the cerebral form often sets in quite sud- 
denly with apoplectiform symptoms ; in the pseudo-bulbar 
paralysis there is a manifestation of other cerebral disturbances 
which do not occur in Duchenne's disease. Again, the latter 
runs an uninterrupted progressive course, while in the cerebral 
paralysis long remissions are frequently met with. A certain 
asymmetry of the paralysis, which is especially noticeable in 
the orbicularis oris (Berger), favors the diagnosis of the cerebral 
as opposed to the bulbar affection. Far more important than 
all these points is the condition of the tongue, which in the 
pseudo-bulbar paralysis does not become atrophied, and hence 
does not assume the appearance so eminently characteristic of 
the true bulbar form. Consequently there are no changes to 
be made out in the electrical excitability, whereas in Du- 
chenne's disease reaction of degeneration is the rule. If, 



252 



DISEASES OF THE BRAIN PROPER. 



finally, we add that in the cerebral form the laryngeal muscles 
seem either to be not at all or only a little affected, we have 
sufficient data to solve the question of differential diagnosis in 
most cases satisfactorily. 

The prognosis with regard to life is just as unfavorable 
in the one as the other form, only this should be borne in 
mind, that in the pseudo-bulbar paralysis remissions may oc- 
cur ; that we therefore can with a clear conscience give the 
patient good hopes of improvement. The duration of the dis- 
ease may be much longer than is ever the case in the genuine 
bulbar paralysis. 

The treatment is not so hopeless, as in Duchenne's disease. 
The galvanic current intelligently applied, and careful galvan- 
ization of the brain and peripheral faradization of the paretic 
muscles, frequent excitation of the muscles of deglutition, as 
was described on page 151, all may be tried with the justifiable 
expectation of effecting at least a transient, sometimes, indeed, 
a quite gratifying improvement. 

LITERATURE. 

Ziegler. Lehrbuch der allgem. und speciellen pathol. Anatomic Bd. ii, Jena, 

1885. 
Polchen. Zur Aetiologie der Hirnerweichung nach Kohlendunstvergiftung 

nebst einigen Bemerkungen zur Hirnquetschung. Virchow's Arch., Bd. 

112, Heft 1, 1888. 
Wachsen. Zur Pathologie der Encephalomalacie. Diss, inaug., Breslau, 1887. 
Moebs. Beitrag zur Pathologie der Gehirnerweichung. Diss, inaug., Breslau, 

1887. 

Pseudo-bulbar Paralysis. 

Jeffrey, A. Marston. Edin. Med. Journ., vii, 1861. 
Joffroy. Gaz. de Paris, 41, 42, 44, 46, 1872. 
Lepine. Revue mensuelle de med. et de chir., 1877. 
Hahn. Ueber Pseudobulbarparalyse. Inaug. Dissert., Breslau, 1880. 
Wernicke, loc. cit., pp. 208 et seq., 1881. 
Kirchhoff. Arch. f. Psych, und Nervenkrankh., p. 132, 1881. 
Ross. Brain, July, 1882. 

Berger, O. Paralysis glosso-labio-pharyngea cerebralis (Pseudo-bulbar paraly- 
sis). Bresl. arztl. Zeitschr., 3 et seq., 1884. 

3. Endarter litis {Syphilitica). 

This process, first accurately described by Heubner in 1874., 
affects more especially the vessels at the base of the brain. 
The walls become opaque, show grayish translucent or whitish 
thickenings, and the vessels finally may be converted into firm, 



ENDARTERITIS SYPHILITICA. 253 

grayish-white cords. The new tissue which encroaches upon 
the lumen of the vessel either originates in the intima by an in- 
crease of the endothelial cells, which become transformed into 
connective tissue (Heubner) or is derived from the nutrient ves- 
sels of the media and adventitia, and consists therefore of emi- 
grated cells (Baumgarten). On account of this tendency to thick- 
ening and consequent obliteration of the vessels, C. Friedlander 
has proposed for the process the name endarteriitis obliterans. 
While not denying that Heubner, who has studied the question 
most carefully, has arrived at important results, we must at the 
same time affirm that the arterial disease, which he describes as 
specific in nature, is not peculiar to syphilis, but that we find the 
same changes wherever we have a chronic inflammatory pro- 
cess with the formation of granulation tissue, as, for instance, 
as a consequence of alcoholism (C. Friedlander). This one 
fact remains of the greatest practical importance, that in the 
course of syphilis the cerebral arteries are very frequently dis- 
eased, and that as the outcome of this diseased state the most 
diverse cerebral symptoms may arise. That under certain cir- 
cumstances a hemianopia can be the result of such disease is 
proved by the interesting case reported by Treitel and Baum- 
garten (Virch. Arch., Bd. cxi, Heft 2, 1888), where, as a con- 
sequence of gummatous arteriitis obliterans of the arteria cor- 
poris callosi dextra, although the optic nerves were intact, a 
unilateral temporal hemianopia had developed. Furthermore, 
it is to be remembered that often enough an autochthonous 
thrombosis due to this arterial disease gives rise to an attack 
which can not be distinguished from the above-described true 
apoplectic stroke with consequent hemiplegia. If recovery 
takes place in these cases the same thing may be repeated sev- 
eral times, and it is especially in syphilitic diseases of the ar- 
teries that this seems relatively frequent. The patient suffers 
from intense paroxysmal headaches, occasionally loses his con- 
sciousness, and presents a transient hemiplegia, but again re- 
covers fairly well, until finally he succumbs to a graver stroke. 
This, then, is the usual course which the disease takes. It can, 
of course, only be diagnosticated where the history of syphilis 
is clear. 

The recognition may sometimes be difficult if other cerebral 
symptoms are present, such as speech disturbances, intention 
tremor, decrease in memory, and the like, when we are liable 
to think of multiple sclerosis, or progressive paralysis of the in- 



254 



DISEASES OF THE BRAIN PROPER. 



sane, and it may only be the amenability of the disease to spe- 
cific treatment which will clear up all doubts. This consists in 
the use of bold doses of potassium iodide, 4.0-6.0 (3 j-3 jss.) a 
day in hot milk until sixteen ounces are taken, and an ener- 
getic course of inunctions — thirty to fifty inunctions of 2.0-2.5 
(gr. xxx-xl) ung. hydrarg. It should be begun as soon as pos- 
sible, as the patient is in no way injured by this procedure, 
while the benefit may be most conspicuous. 

4. Dilatation of the Arteries of the Brain. 

Aneurisms of the cerebral arteries may be of traumatic 
origin or, what is more common, may depend upon endarteri- 
tis, and in this latter case syphilis again deserves special men- 
tion, as among fifty cases of brain syphilis there were found 
six instances with aneurisms (Heubner). Further, there is 
the embolic origin of aneurisms, which must not be forgotten 
(Ponfick). 

Dilatations have been noted in the basilar artery, in the 
middle cerebral, and, though but rarely, in the vertebrals. 
Three cases of basilar aneurism have been reported by Noth- 
nagel (Topische Diagnostik, p. 526); the symptoms presented 
nothing characteristic, but varied much, and even symptoms 
referable to the pons were not in all cases present. Vertebral 
aneurisms, as described by Cruveilhier, Lebert, and others, 
have occasionally been found to be attended with occipital 
neuralgia. Dilatation of the vertebrals produced by atherom- 
atous degeneration may affect the surrounding parts, and, 
as a consequence of structural changes produced in the neigh- 
borhood of the vagus, lead to grave respiratory disturb- 
ances (Oppenheim, Berliner klinische Wochenschrift, 34, 
1887). 

Aneurisms of the ophthalmic or internal carotid in the 
cavernous sinus may give rise to a pulsating exophthalmus, 
which can by appropriate manipulation be temporarily pressed 
back into the orbit. The pulsation of the eyeball, which may 
be propagated to the forehead and temple, is a source of great 
annoyance to the patient. In connection with multiple aneu- 
risms, such as have been observed by Paulicki, for instance, 
existing simultaneously in the basilar, the anterior communi- 
cating, and the middle cerebral artery, epileptiform convul- 
sions and psychoses have been noted. Definite pathognomon- 
ic signs do not, however, exist, and the diagnosis intra vitam 



NEUROSES OF THE CEREBRAL ARTERIES. 255 

is only exceptionally made with certainty. According to Ger- 
hardt, there can at times be heard between the mastoid process 
and the thick cords of the muscles of the neck a murmur refer- 
able to the cerebral arteries ; it is systolic or continuous, and 
is heard on one or both sides if the patient refrains from 
breathing or swallowing. Nevertheless, it is rather excep- 
tional that a (small) aneurism of the cerebral arteries is diag- 
nosticated correctly during life. In larger aneurisms, which 
produce characteristic focal symptoms, this will at times be 
easier, especially when aetiological data — e. g., traumatism — 
are present. 

5. The Neuroses of the Arteries of the Brain {Anczmia and 
Hyper cemia of the Brain). 

The vaso-motor nerves of the cerebral and meningeal arter- 
ies arise partly from the cervical sympathetic (Donders and 
Callenfels), partly from certain cranial nerves (Nothnagel). 
They may be excited or paralyzed idiopathically, or reflexly, 
especially from the stomach, and the resulting conditions, 
although as yet only imperfectly understood, are of great 
practical importance. Both stimulation and paralysis are, of 
course, usually only temporary, while in the intervals and in 
the normal state the vaso-motor nerves as well as their centres 
are in a state of moderate tonus. If the stimulation should 
from any cause be more than is necessary to maintain this 
normal tonus, a spasmodic contraction of the smaller arteries 
takes place, the absolute amount of blood in the brain becomes 
diminished, the patient gets pale, complains of dizziness, and 
loses consciousness — in other words, "faints" (acute nervous 
cerebral anaemia). At the same time the heart's action is weak- 
ened, the pulse is small, the face and body are covered with 
cold perspiration, and if this irritation is frequently repeated a 
certain predisposition to slight changes in the blood-pressure 
becomes gradually established, a condition of things which is 
favored by the mobility of the cerebro-spinal fluid. The at- 
tacks now occur on the slightest provocation, and in the in- 
tervals between them the patients complain of dull headache, 
vertigo, etc., the face at the same time usually being of a pale, 
wax-like color. Certain general diseases, especially chlorosis 
and pernicious anaemia, greatly predispose to these paroxys- 
mal vascular spasms ; in fact, cerebral anaemia is not infre- 
quently one of the symptoms of general anaemia, as it is ob- 



256 



DISEASES OF THE BRAIN PROPER. 



served, for instance, after frequent and profuse bleeding from 
haemorrhoids. 

Among the ^etiological factors, certain occupations play an 
important role. Working in lead especially may give rise to a 
chronic vascular spasm, and thus to cerebral anaemia, which 
is associated with almost constant headache (encephalopathia 
saturnina). 

Tanquerel des Planches, the best modern authority on 
saturnine affections, has described this condition, and it has 
again and again been made the subject of the most careful 
inquiries. It would be beyond the scope of our present work 
to speak of these in detail ; those interested in the subject will 
find references at the end of the chapter ; suffice it only to say 
here that this saturnine anaemia, if the obnoxious action of the 
metal is continued and the disease is once established, may 
produce in the workers severe cerebral attacks, epileptiform 
convulsions, and the like. 

The treatment of acute cerebral anaemia consists primarily 
in placing the patient in an appropriate position — that is, with 
the head low or at about the same level as the feet, so as to 
aid the blood flow to the brain ; the use of stimulants (wine, 
brandy, coffee), occasionally a subcutaneous injection of ether, 
may be indicated. 

For chronic cerebral anaemia galvanization of the brain or 
of the cerebral sympathetic may be tried. As a matter of 
course attention must also be paid to a possible primary cause, 
and every pernicious aetiological factor removed (change of 
occupation, etc.). 

The opposite condition, a paralysis of the vaso-motor 
nerves, produces a dilatation of the cerebral vessels, and thus 
an immediate overfilling of the same. This can be demon- 
strated by ophthalmoscopic examination. Often, but not 
always, the vessels of the face share in the disturbance ; the 
countenance of the patient assumes a purplish-red color, 
he complains of throbbing in his temporals and carotids, 
of headache, of buzzing in the ears (acute nervous hy- 
peraemia) — in general, of about the same symptoms as we 
have described in the vascular spasm, the only difference 
lying in the color of the face. It is observed in certain 
individuals regularly after the use of quite moderate quan- 
tities of alcoholic beverages (wine, beer), or, just as the 
anaemia, after emotions, strong bodily or mental exertion, 



NEUROSES OF THE CEREBRAL ARTERIES. 



257 



too much stud)% etc. ; the abuse of tobacco may also give 
rise to it. 

On account of the very varied manifestations of the affec- 
tion different forms of cerebral hyperemia have been distin- 
guished (Andral, Eichhorst). Thus, a cephalalgic, a psychical, 
a convulsive, and an apoplectic form have been described, ac- 
cording as either headache or psychical excitement, with in- 
somnia or epileptiform attacks or periods of unconsciousness 
(which latter are not rarely followed by cerebral haemorrhage), 
are the most prominent symptoms. The transition between 
these " forms " is, however, so gradual, and so seldom are they 
sharply defined, that, for practical purposes, it does not seem 
worth while to make the distinction. We have repeatedly 
observed marked contraction of the pupils, while in anaemia 
they are more frequently dilated and react sluggishly. As we 
have pointed out above (page 223), simple cerebral hyperaemia 
may produce hemiplegia, which can easily be confounded with 
the apoplectic form (pseudo-apoplexy). 

The treatment is rather unsatisfactory ; it is true we may 
in acute attacks of cerebral hyperasmia give early relief to a 
patient by placing him in an appropriate — that is, nearly sit- 
ting — posture, by applying ice-bags to his head, or, finally, by 
free venesection ; but these attacks are so frequently repeated 
in individuals predisposed to them that the question of such 
treatment is not of so much importance as of the adoption for 
months and years of a careful dietetic regime. Besides keeping 
the bowels well open — a thing which should never be omitted 
— the patient must be advised to take enough exercise, even 
practice gymnastics ; he should be cautioned against indul- 
gence in heavy, indigestible foods, and, above all, in alcoholic 
beverages. A yearly visit to places like Marienbad, followed 
by a stay in a pure mountain air, moderate but daily excur- 
sions on foot, the occasional use of Carlsbad water under the 
direction of the physician — all these may be prescribed with 
advantage. Much care should, however, be taken with the so- 
called cold-water treatment, which, like sea-baths, may only 
increase the hyperasmia. This applies equally to the massage 
treatment, which, unless carried out in accordance with certain 
indications and fixed rules, and under the supervision of a com- 
petent medical man, often is productive of more harm than 
good in this disease. 



258 



DISEASES OF THE BRAIN PROPER. 



LITERATURE. 



Tanquerel des Planches. Lead Diseases ; with Notes and Additions on the Use 

of the Lead Pipe and its Substitutes. By Samuel L. Dana, Lowell, 1848, 

and Boston, 1850. 
Revillout. Gaz. des hop., 68-71, 1873. 
Berger, O. Berl. klin. Wochenschr., xi, 14, p. 122, 1874. 
Malassez. Gaz. de Paris, 1, 2, 1874. 
Brochin. Gaz. des hop., 24, 1875. 
Lepine. Gaz. de Paris, 47, 1875. 
Hirt. Krankheiten der Arbeiter, iii, 49, 1875, 
Haueisen. Wiirtemb. Corresp. Bl., li, 36, 1881. 
Ullrich. Zur Encephalopathia saturnina. Allg. Zeitschr. f. Psych., xxxix, 2, 3, 

1882. 
Charlier. Contribution a l'etude pathog£nique du saturnisme cerebro-spinal. 

These de Paris, No. 201, 1882, pp. 45 et seq. 
Schulz, Paul. Ueber Encephalopathia und Arthralgia saturnina. Diss, inaug. 

Vratislav, 1885. 
Corning. New York Medical Record, November 13, 1886. 
Langeveld. Hyperhemie chronique du cerveau et de la moelle epiniere. Progr. 

med., No. 28, 1887. 

B. Diseases of the Cerebral Veins and Sinuses.— The blood 
from the brain and meninges is carried back toward the heart by the 
internal jugular vein. This vessel emerges from the jugular fora- 
men and after its junction with the external jugular becomes the 
common jugular, which, after it has in turn recei ed the subclavian, 
is called the innominate vein. The two innominates together form 
the superior vena cava. 

Between the two layers of the dura mater there exist spaces 
which convey venous blood but are without valves. These are 
called sinuses. The veins of the cortex empty themselves into the 
longitudinal sinus (sin. falcif. maj.), which terminates behind in the 
torcular Herophili (confiuens sinuum). The mode in which the veins 
empty into the sinus — namely, in the direction opposite to that of 
the blood current in the latter — produces a slowing of the circula- 
tion, and thus explains the frequent occurrence of coagula in the 
veins of the cortex and the sinus. The deep cerebral veins are col- 
lected into two trunks, which are known as the veins of Galen. 
These again unite into one, the vena magna Galeni. They convey 
the blood from the ventricles to the sinus rectus sive perpendicu- 
laris, which in its turn empties itself into the torcular Herophili. 
The blood from the inner ear goes into the cavernous sinus which is 
situated at the side of the sella turcica; that from the mastoid cells 
into the lateral sinus, which at the jugular foramen passes into the 
so-called bulb of the internal jugular vein. The veins themselves 



DISEASES OF THE CEREBRAL VEINS. 



259 



anastomose but little with each other, while the sinuses do so freely. 
It is important to note the communications between the intracranial 
and the extracranial veins — for instance, of the nasal with the ante- 
rior end of the longitudinal sinus, the ophthalmics with the sinus 
cavernosus and the facial veins, etc. — and the communications made 
by the venae diploeticae, for only then can we understand how patho- 
logical processes can extend from the outside of the skull to the in- 
side, and how occasionally we find an external swelling in affections 
of the sinuses. 

Here it is more especially thrombosis with which we have 
to deal, which may occur in the veins as well as in the sinuses. 
The distinction is not always easy in life nor even after death, 
because after death the venous thrombosis may extend into 
the sinus and be taken for a sinus thrombosis. 

If only one vein is affected the mischief may be but slight. 
Usually, however, it takes in one or two of the larger veins, 
which become obstructed during the course of exhausting, 
acute, especially infectious diseases or after an injury, for in- 
stance, a blow on the head. The preponderating number of the 
patients are children, and at times, especially during the hot 
season, quite young children, in which cases a special astiolog- 
ical datum can not be found. The symptoms are the follow- 
ing : Hemiplegia, ushered in by convulsions and lasting only a 
few weeks, is followed by a permanent weakness, not infre- 
quently by occasional spasms in the arm. The development 
of the child is then usually faulty, for apart from the occasional 
atrophy in one arm or in one leg or of the whole side, epilep- 
tiform convulsions may persist for years, which not rarely have 
an injurious influence on the mental development of the patient. 
In such cases at the autopsy often thrombosis of the longitu- 
dinal sinus and of the veins emptying into it is demonstrable. 
In adults, such a thing as a thrombosis of the cortical veins is 
extremely rare. 

Sinus thrombosis may have one of two causes. Either we 
have a general disease which favors the coagulation of the 
blood — as in children profuse diarrhoea, acute infectious dis- 
eases, in old people, tuberculous and carcinomatous processes — 
or neighboring parts, as, for instance, the skull bones or the 
skin of the scalp are diseased (erysipelas), an extension of the 
process becoming possible on account of the communications 
between the extracranial and intracranial vessels above de- 
scribed. We distinguish the true inflammatory thrombosis, 



2 6o DISEASES OF THE BRAIN PROPER. 

which affects the lateral, the petrosal, and the cavernous sinus, 
from the so-called marantic thrombosis, which often occurs in 
the superior longitudinal sinus. In both cases the secondary 
symptoms of engorgement, which are especially marked in 
thrombosis of the longitudinal sinus and which manifest them- 
selves in so-called meningeal haemorrhages, are of the greatest 
importance. Such meningeal haemorrhages are found in chil- 
dren (post mortem) as thick coagula distributed over the cor- 
tical motor centres, where they have in life given rise to a 
curious combination of paralysis and spasm, the power of 
spontaneous movements, however, being retained (Gowers). 
Choreic movements complete the picture which congenital 
chorea, bilateral athetosis, and double spastic hemiplegia pre- 
sent, cases which are difficult to interpret and still more diffi- 
cult to diagnosticate. In these patients, too, the mental devel- 
opment remains imperfect, and their irregular movements and 
contractures (often most marked in the calf muscles) give them 
the appearance of helpless cripples. 

The diagnosis of sinus thrombosis can only be made with 
any certainty if to the general symptoms (headache, somno- 
lence, paralyses in the distributions of the cranial nerves) signs 
are added which point to circulatory disturbances peculiar to 
sinus thrombosis. Thus, for instance, symptoms of engorge- 
ment in the ophthalmic veins, manifesting itself by prominence 
of the eyeball, oedema of the lids, congestion of the retina, etc., 
point to obstruction of the cavernous sinus ; ©edematous swell- 
ings behind the ear to affections of the lateral sinus, and finally 
symptoms of passive hyperaemia in the nose — epistaxis, marked 
fullness in the veins of the temporal region, in small children 
fullness of the anterior facial veins situated between the large 
fontanelle and the temples (Gerhardt) — to implication of the 
longitudinal sinus. Pain and swelling of the corresponding 
side of the neck may be significant of a jugular thrombosis, 
etc. All these conditions are, however, but rarely met with, 
and they are more easily found in the books than demonstrable 
in the patient. The duration of a sinus thrombosis varies be- 
tween several days and three to at most four weeks. The 
prognosis is usually unfavorable and the treatment unsatis- 
factory and purely symptomatic. 



BRAIN ABSCESS. 261 



INFLAMMATORY PROCESSES IN THE BRAIN SUBSTANCE. 

/. Purulent Encephalitis — Brain Abscess. 

Pathological Anatomy. — Circumscribed pus formations in 
the substance of the brain, which anatomically differ in no way 
from pus formations in other organs, are called brain abscesses, 
and we speak of them as encapsulated and non-encapsulated, 
according as to whether or not they are definitely separated 
from the surrounding tissues by sclerotic thickening. In the 
former, a membrane of connective tissue incloses the abscess, 
which contains a thick pus ; in the latter, disintegrated nerve 
tissue and crystals of cholesterin are found in conjunction with 
the frequently very foetid pus, and the abscess -walls are formed 
by a soft layer of brain tissue infiltrated with pus, and sur- 
rounded by areas of yellowish softening and oedema. In the 
softened areas compound granular corpuscles are found in 
great numbers. The size of the abscess may vary from that 
of a pea to that of an apple, and it may even take in nearly the 
whole hemisphere. The larger the abscess the more marked 
are the signs of increased intracranial pressure, the more flat- 
tened and indistinct the convolutions on the surface of the 
brain, and the drier and more adherent becomes the pia mater. 
Should the abscess break through into one of the ventricles 
pus may eventually be found in all of them, and the ependyma 
then appear cedematous. If it reaches the surface of the brain 
it may give rise to a diffuse purulent meningitis (Wernicke). 

Etiology. — -^tiologically, injury is of the greatest impor- 
tance, though it need not necessarily have affected the skull 
itself, but may produce an abscess just as well if confined to 
the soft parts ; in such a case, the inflammation extends through 
the bone, and the infectious material penetrates into the brain 
from the flesh wound. If we have no open wound, no break of 
continuity in the soft parts, then even extensive destructions of 
the brain substance often do not lead to an abscess formation, 
just as in the fractures of the skull healing occurs without sup- 
puration if only the external air is excluded from the injured 
parts of the brain. 

Besides traumatism, suppuration occurring in the neigh- 
borhood of the brain may cause a brain abscess ; thus, in 
rare instances, it is a purulent parotitis or suppuration in the 
nasal cavity or, more frequently, caries of the petrous portion 



2 62 DISEASES OF THE BRAIN PROPER. 

of the temporal bone or suppuration in the middle ear which 
becomes the starting point. For years an otitis media may- 
persist and be attended with a purulent discharge from the 
external ear without any brain symptoms, but suddenly this 
running may stop, the pus is retained, and probably gives rise 
to the caries of the bone, on account of which the petrous por- 
tion may become so soft that it can be cut with the knife ; a 
brain abscess then develops either in the temporal lobe or in 
one of the hemispheres of the cerebellum. 

Suppuration in the bronchi, putrid bronchitis, bronchiecta- 
sis (Biermer), furthermore, ulcerative endocarditis and pyaemia 
may also give rise to brain abscesses, which are then desig- 
nated as " metastatic " abscesses. Idiopathic abscesses — that 
is, those in which no ^etiological factor could be discovered 
— have been observed by Striimpell in some cases of epidemic 
cerebro-spinal meningitis. 

Symptoms. — The symptoms of a brain abscess are divided 
into general and focal. There may, however — and this is of 
much practical importance — be no sign of brain mischief at alt. 
A man may not complain of anything worth mentioning, save, 
perhaps, of an occasional headache, and at the autopsy a brain 
abscess be discovered. Quite a number of these cases are 
well authenticated, and there can be no doubt as to their ex- 
istence ; to be sure, we ought not to forget to add that the 
place in which such an abscess is developed must be in a so- 
called indifferent region. 

Among the general symptoms the one most constant and 
the most distressing to the patient is headache; it can by no 
means always be localized, but more frequently affects the 
whole head, and may last with greater or less severity for 
weeks or even months. Occasionally the torture is such that 
the patient, incapable of doing anything, is forced to remain 
quietly in bed. although no other symptoms may be present. 
Very often, it is true, disturbances of the sensorium may ap- 
pear after the headache has lasted for a long time ; a strange 
apathy takes possession of the patient, his sleep is disturbed, 
and his general condition is aggravated if, as is common, 
febrile movements set in, which may be attended with convul- 
sions, which are mostly unilateral. Attacks of vertigo, some- 
times severe enough to cause great anxiety, and sometimes 
only transient, occur, and not rarely there are spells of vomit- 
ing, sometimes lasting for days, and acting very deleteriously 



BRAIN ABSCESS. 263 

on the patient. The ophthalmoscopic examination, as a rule, 
does not reveal any fundus changes ; choked disks are only 
exceptionally found, certainly much more rarely than in brain 
tumors. The focal symptoms of cerebral abscess are almost 
exclusively direct. This is a fact which is easily understood if 
we consider their mode of origin ; they are produced either 
by a direct destruction of the brain substance or by the pre- 
ceding oedema and the attendant " preparatory softening " 
(Wernicke), both of which processes are strictly local. At the 
same time we must not lose sight of the fact that the part 
affected by this " preparatory softening " is still capable of 
regeneration. Indirect focal symptoms have only been ob- 
served in cerebellar abscesses ; in such, paralyses of the abdu- 
cens and other nerves have been noted (Wernicke). 

How different focal symptoms show themselves, and which 
are characteristic of lesions of the different parts of the brain, 
has been discussed above (page 192); suffice it here to add 
that abscesses of the so-called motor region produce hemi- 
plegias, which appear in a very characteristic manner — namely, 
step by step. In abscesses of the occipital lobe hemianopia is 
the direct focal symptom which, if properly used, may settle 
the diagnosis. The direct focal symptom of the temporal lobe 
— the crossed deafness — can only rarely be accurately deter- 
mined, as the suppuration of the middle ear, which we have 
shown often to be serologically connected with brain abscess, 
is mostly bilateral, and as testing of the hearing in patients, 
whose mental activity is somewhat dulled, is very difficult, 
since they are usually unable to appreciate any decrease in 
hearing on one side. In general, we must confess that too little 
attention has been paid to the testing of the hearing, and that 
the examinations have not been made with sufficient care. 

In no one of the few reported cases of abscess of the pons, 
the medulla oblongata, and the cerebellum have direct t focal 
symptoms been observed, or at least noted with any certainty ; 
the general symptoms, which are mentioned in connection 
with the abscesses of the cerebellum, must be attributed to 
pressure produced by the growing abscess. 

Course. — The disease may pursue its course in one of three 
different ways : 

(1) It assumes from the onset a tumultuous character, 
whether it originate from a traumatism or disease of the mid- 
dle ear. Violent pains — at first local, later spreading over the 



264 DISEASES OF THE BRAIN PROPER. 

whole head, and lasting from two to four days — together with 
marked elevation of temperature and paroxysms of convulsions, 
are followed by grave disturbances of consciousness. These 
may last for three, four, even eight days, when the patient, 
without regaining consciousness, dies in a restless delirium, 
presenting the picture of one suffering from severe organic 
disease. 

(2) These paroxysmal symptoms lose, after a few weeks, 
their acute character, and become less and less marked ; the 
patient seems to feel better, and he may, indeed, be free from 
all trouble for several months. Even the headache seems — at 
least at certain times — to have vanished. This state of absolute 
(or relative) latency may be of variable duration, and may, by 
the inexperienced diagnostician, be mistaken for complete re- 
covery, but it is doubtful whether this latter ever occurs. It 
certainly happens much more frequently that after this period 
of latency the initial symptoms again make their appearance, 
this time to continue without intermission until death. The 
duration of the whole disease comprises then three to six 
months or more ; it is extremely rare that the period of latency 
lasts for years. 

(3) The onset of the disease is insidious and chronic. The 
patient, who presents slight fever and general symptoms, grad- 
ually becomes emaciated. He complains of headache and dis- 
turbed sleep, and from time to time, apparently without reason, 
is taken with chills ; he begins to have a cachectic appearance 
and bears on his face the imprint of a grave disease. In such, 
withal very rare, cases our patient is suffering from phthisis 
and the brain abscess is of a tubercular nature. The duration 
of this form, as a rule, does not exceed three or four months. 

Diagnosis. — In the diagnosis we may have to differentiate 
between brain abscess, purulent meningitis, meningeal haemor- 
rhage, and brain tumor. If the course of the abscess is very 
acute, as has been described above (eight to ten days), then it 
is often impossible to distinguish it from an acute purulent 
meningitis, an error which is the more excusable when all direct 
focal symptoms which often accompany an abscess are wanting. 
Remissions point rather to the existence of a brain abscess. 

From meningeal haemorrhage, which just as abscess may 
be the consequence of traumatism, it is also distinguished by 
its course. Traumatic meningeal haemorrhages usually give 
rise to epileptiform attacks, which are to be referred to the 



BRA IN ABSCESS. 



265 



effect of the entrance of the blood between the dura and the 
skull on the motor centres. They are immediately followed 
by a coma, which lasts until death. In abscesses the insensi- 
bility usually lasts only a few hours, and only after a marked 
improvement has again taken place do alarming symptoms 
make their appearance. 

A brain tumor can be differentiated from an abscess by the 
fact that in the former febrile symptoms are absent, while, on 
the other hand, in the latter, choked disks, which are a fre- 
quent sign in brain tumor, are only exceptionally noted. The 
course — more especially as regards the remissions, which are 
well marked and often of long duration — is characteristic of 
abscess ; a tumor usually is steadily progressive. Finally, we 
are justified in diagnosticating an abscess if after a protracted 
and varying course the disease suddenly terminates with cer- 
tain severe symptoms of collapse and death. When this occurs 
it is probable that an abscess existed which has perforated 
either into the ventricles or to the surface. In cases of trauma- 
tism or in cases in which the cerebral symptoms were preceded 
by an otitis media we should always think first of brain abscess. 

The seat of the abscess can only then be determined with 
any certainty if characteristic focal symptoms— for instance, 
hemianopia or sensory aphasia — are present. In cases of hemi- 
plegia we can, from the order in which the component mono- 
plegias occur, draw a conclusion as to the point of origin of 
the abscess. Thus, if at first a paralysis of the leg, together 
with marked sensory disturbances, are the prevailing symp- 
toms, and only later the arm and facio-lingual region become 
affected, we may conclude that the abscess is proceeding from 
behind forward, while if the symptoms occur in the reverse 
order, then the frontal lobe may have been the starting point 
and the abscess be extending backward. In cases of traumatism 
the abscess is to be located in very close proximity to the injury. 
Where there is a history of otitis media it usually establishes 
itself in the temporal lobe or the cerebellum. The white mat- 
ter is, in the cerebrum as well as in the cerebellum, by far the 
most common seat. In the brain stem it occurs only very 
rarely, while in this situation, as we have seen, haemorrhage 
and softening are more common. 

Prognosis. — The prognosis is absolutely bad with regard to 
recovery and doubtful with regard to life. We can see from 
what has been said that spontaneous cures, most probably never, 



2 66 DISEASES OF THE BRAIN PROPER. 

therapeutic cures quite rarely, take place. It is well to be very 
guarded in giving an opinion as to the duration of life, and we 
should never forget that even during a seemingly excellent 
state of health suddenly grave symptoms may develop which 
lead to a rapid termination. 

Treatment. — Of an effectual treatment we can only speak 
in those cases in which an operation is feasible. Since this — 
trephining of the skull, splitting of the dura, opening of the 
abscess with the knife — must always, however, even if con- 
ducted with the strictest antiseptic precautions, be regarded 
as a grave undertaking, we should only resort to it when the 
location of the abscess has been established with some cer- 
tainty. If this has been done, operative measures are at once 
indicated, and should be carried out without delay, provided, 
of course, that the abscess be in a part accessible to the knife, 
which, we need not say, is hardly the case in the basal ganglia, 
the pons, the medulla oblongata, and the cerebellum. 

But, unfortunately, an operation is in the greater number 
of cases not feasible on account of the uncertainty in the top- 
ical diagnosis. Then our treatment can only be symptomatic, 
and we are confined to local bleeding, hypnotics, bromides, 
etc., which effect but little. For that matter the results of a 
so-called successful operation are not always lasting either, 
and repeatedly one, two, or four weeks after the pus has been 
evacuated an unfavorable outcome has taken place — e. g., in 
the case of Wernicke-Hahn (cf. lit.). 

LITERATURE. 

Wernicke and Hahn. Idiopathischer Abscess des Occipitallapens durch Tre- 
panation entleert. Virchovv's Arch., Bd. lxxxvii, 1882. 

Greenfield. Remarks on a Case of Cerebral Abscess with Otitis, successfully 
treated by Operation. Brit. Med. Journ., 12, ii, 1887. 

Frankel, A. Ueber den tuberculosen Hirnabscess. Deutsche med. Wochen- 
schr., 18, 1887. 

Sommerville. Analysis of the Urine in Two Cases of Cerebral Abscess. Lan- 
cet, ii, 12, 1887. (Increase of the earthy phosphates.) 

Link. Traumat. Gehirnabscess. Wien. med. Wochenschr., No. 50, 1887. 

Rossa. New York Med. Record, xxxii, July 5, 1887. (Brain abscess in conse- 
quence of a purulent otitis media.) 

Lacher. Munchener med. Wochenschr., xxxiv, 33, 1887. 

Barr. Glasgow Med. Journ., xxviii, September 3, 1887. (Very protracted 
course — long intermissions.) 

Bergmann, v. Die chirurgische Behandlung von Hirnkrankheiten. (Brain ab- 
scess, etc.) Arch. f. klin. Chirurgie, Bd. 36, 4, 1887. 



DIFFUSE CEREBRAL SCLEROSIS. 



267 



2. Nonsuppurative Encephalitis and its Consequences (''Athetosis "). 

A. IN ADULTS. 

There is no question but that inflammatory processes, acute 
as well as chronic, occur in the brain which show no tendency 
to suppuration, although our knowledge of their pathogenesis 
and their symptomatology is very imperfect. These processes 
take place preferably in quite early childhood, or even during 
intra-uterine life ; only exceptionally may they occur in adults, 
as a consequence of the abuse of alcohol. They are then cir- 
cumscribed inflammatory processes, occurring partly in the 




Fig. 82.— Porencephaly. 



cortex, partly in the white matter which admit of regeneration. 
If larger areas are affected, the tissue becomes shrunken and 
of a distinctly firmer consistence, so that it cuts almost like 
leather. Just how these changes are brought about, in what 
way the nerve fibres of the white matter waste and the con- 
nective tissue increases, which of the two processes is the pri- 
mary and which the secondary, can not as yet be determined 
with any certainty. Peculiar disturbances in nutrition in cer- 
tain areas of arterial distribution may give rise to defects 
which cause a distinct sinking in of the surface of the brain 
(Kundrat), "porencephaly" (Fig. 82). At times we find a true 
cicatricial tissue, which characterizes the terminal process of the 
diffuse cerebral sclerosis. The macroscopic appearance of the 
brain is similar to that in the 



induration cartilagineuse " of 



2 68 DISEASES OF THE BRAIN PROPER. 

Cruveilhier ; microscopically, the same histological elements as 
are seen in all degenerative processes of the gray and white 
matter of the brain, spider cells, and compound granular cor- 
puscles, are noted (Kast). Marie and Jendrassik (cf. lit.) see 
in perivascular changes the chief factor which under certain 
circumstances brings about a lobar atrophy. At times we 
have to deal undoubtedly with the consequences of a uniform 
arrest of development which especially takes in one hemi- 
sphere and the anatomical cause for which is not understood. 
The circumscribed inflammatory foci may also be found in 
both hemispheres, in which case we speak of a double lobar 
sclerosis. 

The clinical course of the disease is practically unknown. 
Probably there does not exist any well-defined constant clinical 
picture, but the symptoms vary according to the anatomical 
seat of the process. They are symptoms of paralysis or of irri- 
tation, and are partly " cortical symptoms " and partly to be 
referred to disease of the cerebral vessels. In the few cases in 
which a diagnosis could be made during life, apoplectiform at- 
tacks, rhythmical choreic movements, longer or shorter spells 
of unconsciousness, were observed. The difficulty of grouping 
and correctly interpreting the symptoms is chiefly owing to 
the impossibility of an early diagnosis. Hence it will be the 
chief task of future observers to direct their attention to the 
initial stage, for only after we have once become familiar with 
the development and the anatomical changes in this first stage 
can we hope to elaborate an efficient mode of treatment, w T hich, 
we need not say, at present is absolutely wanting. The irra- 
tional trials with potassium iodide we can certainly not regard 
as such. 

B. IN CHILDREN. 

Cerebral Palsy of Children — Hemiplegia Infantilis Spastica {Bene- 
dict) — Polio-encephalitis {Striimpell). 

Pathological Anatomy. — In view of the comparatively fre- 
quent occurrence of cerebral palsies in children, it is rather 
to be wondered at that so extremely little is known about 
their pathogenesis and their initial stage, more especially with 
reference to the anatomical changes that occur. This may, 
perhaps, be accounted for by the difficulty, and sometimes 
even impossibility, of making an early diagnosis. At a time 
when we are able to recognize the disease we usually have to 



CEREBRAL PALSY OF CHLLDREN. 269 

deal with a process which has already passed through all, 
or almost all, of its different stages. It is the same with the 
lesions which we find : they in no wise explain the exact 
nature of the disease, but only give us an idea of the many 
various ways in which the brain with its meninges may be 
altered in early childhood as a consequence of the disease, 
which was most probably intra-uterine. We do not, however, 
know of what nature this process is, whether it is a sinus 
thrombosis, as Gowers claims, or an inflammation leading to 
atrophy, as in meningo-myelitis chronica. Neither can we tell 
whether the increase in the connective tissue which has been 
noted by many authors is a primary one, and what part the 
disease of the vessels, the thickening of their walls (Hayem, 
and others), plays in the process ; but one thing is certain, 
that the disease is not confined to the gray cortex alone (as 
Striimpell has assumed, and for which reason he has proposed 
the name polio-encephalitis, analogous to polio-myelitis, cf. lit.), 
but that the white matter as well may be implicated. This is 
shown by the case published by Kast (cf. lit.), and also by the 
following observation, which was made in my wards, and which 
I propose to relate here in brief, as autopsies in cases of this 
class are rare : 

Magdalena St., twenty-one years old, coming from a healthy fam- 
ily, was taken sick in her second year with violent fever. Accord- 
ing to her mother's account, she had convulsions for four days and 
four nights. When she wanted to get out of bed after this her left 
side was found to be paralyzed. Inside of three months her condi- 
tion was so far improved that she could walk, although with a limp. 
Gradually the left lower leg became smaller and somewhat curved, 
and she complained of pain in the whole limb. The upper extrem- 
ity did not at first take part in the atrophy; it was, however, almost 
completely powerless. For two years the convulsions did not re- 
appear ; but for the last four years the patient has had, on an aver- 
age, about one epileptiform attack every three weeks, in which she 
bites her tongue and passes her urine involuntarily. The following 
is an extract of the note made on October 25, 1885 : 

Head : Right parietal region painful to percussion ; in the region 
of the left glabella and the hairy part of the scalp, on the same side, 
there are several areas of anaesthesia. Pupillary reactions and move- 
ments of the eye muscles normal. Nothing abnormal in the distribu- 
tion of the facial and hypoglossal nerve. On the right side hearing 
is much below normal, on the left there is complete deafness. On 



270 



DISEASES OF THE BRAIN PROPER. 



the anterior third of the left half of the tongue taste is lost. Uvula 
straight and movements of soft palate normal. 

Trunk : On the left half of the chest touch and the prick of a pin 
are not perceived ; temperature sense seems decidedly subnor- 
mal. 

Upper Extremities: The whole left upper extremity, including 
the hand, is shorter and smaller than the right ; motion of the wrist, 
especially extension, is impaired. The hand is flexed on the fore- 
arm, and only with force can the flexion be overcome. The thumb 
is drawn into the hollow of the hand, the rest of the fingers are 
slightly flexed. Motion in the shoulder joint normal ; in the elbow 
joint extension is slightly impaired. There is a general decrease in 
the sensibility. Electrical reactions are found to be normal for both 
currents, on direct as well as on indirect stimulation. The right 
upper extremity does not show abnormity with regard to develop- 
ment, size, mobility, or sensibility. 

The left lower extremity is considerably smaller and shorter than 
the right; sensibility is the same as in the corresponding upper ex- 
tremity ; the same holds for the electrical condition. Tendon and 
skin reflexes are retained on both sides. 

The epileptic attacks continued, and occurred about every sixth 
or eighth day ; the intelligence became more and more impaired. A 
tuberculous process in the left lung was superadded to the already 
existing trouble, and, in consequence of general failure of strength, 
the patient died on March 22, 1886. 

Autopsy : Eighteen hours after death. Extract from the post- 
mortem record : After opening the skull the pia is seen to be con- 
siderably thickened at different places, especially over the right 
hemisphere In volume the right hemisphere is not much smaller 
than the left ; the anterior and posterior central convolutions on the 
right side, especially in their lower half, are markedly atrophic, the 
gyri are shrunken to about a third of their natural size ; the infra- 
marginal lobule and the angular gyrus present the same atrophic 
condition. The upper right parietal lobule is less atrophic, never- 
theless the gyri are here also remarkably narrow. The portions of 
the first and second frontal convolutions bordering on the central 
convolution appear also atrophic. On section the gray matter is 
seen to be considerably diminished. 

The ventricles appear markedly enlarged. On frontal sections, 
after Pitres' method, no important changes, with the exception of 
the shrinking, either in the centrum semiovale or in the basal gan- 
glia, can be observed macroscopically ; on microscopical examina- 
tion spider-cells and fat-granules are found in considerable numbers 
not only in the gray cortex, but also in the white matter. 



CEREBRAL PALSY OF CHLLDREN. 271 

This observation determines us in maintaining with Kast 
the old designation, " cerebral palsy of children," a name by 
which no definite pathological change is implied, and in aban- 
doning the term polio-encephalitis, to which the pathological 
changes do certainly not always correspond, especially as the 
latter name has already been proposed by Wernicke for the 
disease of the gray matter around the third and fourth ven- 
tricles. 

Symptoms. — While the anatomical changes at the onset of 
the disease are obscure, the clinical symptoms are quite dis- 
tinct and striking. The disease usually sets in brusquely, the 
symptoms are violent and can not be overlooked. The child 
is seized with a high fever; soon, sometimes only a few hours 
later, twitchings — at first only in one extremity, later in the 
whole side — appear ; at times the whole body may be con- 
vulsed ;• this may last, with but slight interruptions, for from 
one to three, or even four days, and be accompanied by per- 
sistently high temperature. The symptoms now abate, the 
convulsions become less frequent, but after their disappearance 
the child is found to have lost the use of the limbs of one side 
— hemiplegia infantilis. If an early and careful examination be 
made, a moderate facial paralysis is noted, the condition of the 
extremities being very nearly the same as has been described 
on page 228. Here, as in the common cerebral hemiplegia, the 
arm is pressed against the thorax, the forearm flexed at right 
angles with the upper arm, the hand flexed and adducted, the 
fingers bent. The leg is slightly flexed at the knee-joint, the 
foot extended ; not uncommonly the big toe is in marked dorsal 
flexion. The sensibility is, as a rule, not much altered. After 
several weeks the little patient regains enough power to per- 
form the coarser movements with the leg, while for a consider- 
ably longer time the arm does not take part in the improve- 
ment. If the child was able to walk before the onset of the 
disease it will generally regain this faculty after a time, but its 
gait will always be halting. 

The further course of the disease is not the same in all 
cases, and it has been our experience that it differs according 
as the initial convulsions continue or cease. This, therefore, is 
an important point to consider in the prognosis for the relative 
recovery. It will also decide the question whether the child, 
while bodily more or less a cripple, is in addition to be men- 
tally defective and totally useless to the community. What 



272 DISEASES OF THE BRAIN PROPER. 

conditions determine the continuance of the convulsions, 
whether this is influenced more by the nature of the lesions 
or more by their seat, we are unable to say. 

As a rule, the attacks, even if they should have a tendency 
to continue, do not recur for months, for one, two, or even 
four years, after the acute period of the disease has passed 
off. Then, however, they may return on any provocation — 
after a fright, maltreatment, sometimes during- the second den- 
tition — at first at long intervals of months, then more frequently. 
At first they may be slight and of short duration, then more 
severe, until finally they resemble in every point the classical 
attacks of epilepsy — in other words, the hemiplegic or hemi- 
paretic patient has now become an epileptic. As has been 
stated, the influence which these attacks have upon the mental 
development of the child is very detrimental. Much more 
often than is the case in idiopathic epilepsy does the patient 
become weak-minded. The condition of speech found in this 
disease is interesting. If the patient had fully acquired speech 
previous to the attack, it is only affected if the lesion is on the 
left side of the brain, in which case the symptoms do not differ 
from those which we have described under left-sided cerebral 
haemorrhage. If, on the other hand, the patient has not yet 
learned to speak, he will, in case the fits continue, either not 
learn at all or only very imperfectly, and his talk will, even if 
his mind is only slightly impaired, be quite unintelligible ; but 
often the attacks do not recur, so that the mental development 
progresses normally. In such cases speech likewise reaches a 
gratifying degree of development even if it had not yet been 
fully acquired or had again been lost. The healthy hemisphere 
takes on vicariously the work of the injured one (cf. page 181, 
remarks on aphasia of children). 

Independently of the epileptiform attacks there may occur 
changes in the extremities, which are in a way analogous to 
those described on page 228. An especially characteristic 
symptom is the pronounced spastic condition which manifests 
itself in an increase of the reflexes, rigidity and spasm of the 
muscles — hemiplegia infantilis spastica. This rigidity is espe- 
cially well marked in the muscles of the hand and the calves, 
and leads, preferably in the former location, to contractures, 
which, however, differ from others inasmuch as they cease 
during rest and sleep and only appear on voluntary motion, 
Benedikt, above others, has pointed out that at one time one, 



CEREBRAL PALSY OF CHILDREN. 



273 



at another time another, group of muscles may be affected; 
that, e. g., in walking the foot may be held normally, while 
again in the same foot we may see a talipes calcaneus, or at 
another time a talipes equinus. Similar conditions are ob- 
served in the hands ; thus the fingers, which appear to be in 
a state of immobile flexor contraction, may at other times pre- 
sent a remarkable degree of mobility. Under what circum- 
stances contractures appear, why sometimes they are present, 
sometimes absent, is not known. Perhaps the extent of the 
cerebral lesion and the secondary degeneration in the cortico- 
muscular tract depending on this has something to do with it. 
We shall shortly discuss carefully the entirely involuntary 
movements of the affected hand which are noted in the course 
of this disease. 

In almost all cases of infantile cerebral paralysis an arrest 
of development or growth becomes apparent in the affected 
extremities. This may be only insignificant, so as to be hardly 
appreciable. On the other hand, the limbs may in all their 
dimensions be considerably smaller than the corresponding 
ones of the sound side. Occasionally the whole half of the 
body, trunk and head as well, share in this arrest, and we have 
what is called a general hemiatrophy. 

The following illustrations of cases from my clinic repre- 
sent different types of the cerebral paralyses of children : 

Figs. 83 and 84 : Hemiatrophy of the whole left side of the 
body. Epileptiform attacks. Dementia. 

Figs. 85 and 86 : Hemiatrophy of the whole left side of the 
body. Cause : Traumatism. No fits. Intelligence normal. 

Fig. 87 : Atrophy of the left upper and lower extremity 
(resection of the knee-joint). Epileptiform attacks, with a mod- 
erate degree of dementia. 

Figs. 88 to 91 : Atrophy of the paralyzed side, very slight, 
but perceptible. All three patients suffer from epileptiform 
attacks and are demented. All three present contractures on 
the affected side, either in the wrist (Fig. 88 and also Fig. 83) 
or in the ankle-joint (Figs. 90 and 91). 

All these eight cases, which came under my observation, 
depended upon disease of the right hemisphere. Whether this 
side is altogether more frequently attacked, and, if so, how the 
fact is to be explained, I dare not at present decide. 

Diagnosis. — The diagnosis of the disease is, as a rule, easy, 
as the acute onset with the consequent hemiplegia is charac- 
18 



274 



DISEASES OF THE BRAIN PROPER. 



teristic enough ; but if the patient come from a phthisical 
family and is himself tuberculous some doubt may arise. We 
may have a case of tuberculosis of the brain to deal with, 
which sometimes resembles in its onset the cerebral palsy of 






Fig. 83. 

children. High fever and convulsions are not absent and 
severe motor disturbances occur also. The fact, however, that 
in cerebral tuberculosis generally the base of the brain with 
its nerves, especially the oculo-motor and abducens, are impli- 
cated, and, further, that it runs a rapid and fatal course, will 
enable us to make a correct diagnosis. 

Spinal and cerebral infantile paralyses can not be con- 
founded with each other if we keep in mind that in the latter 
one whole side of the body is affected ; that the muscles are 
rigid, the reflexes increased ; that convulsions occur not only 



CEREBRAL PALSY OF CHLLDREN. 275 

at the onset, but also in the further course of the disease ; that 
the mind becomes impaired, etc. In the spinal form, either 
one limb alone — arm or leg — is affected or both arms or both 
legs, and the reflexes in the paralyzed extremities are lost, 




The patient, who is now thirty-six years old, was taken ill in early childhood 
with an acute violent fever and convulsions ; the latter lasted for several days, 
but after that disappeared. From that time the left side did not develop as well 
as the right, so that now the left upper extremity, which can be moved, with 
difficulty only, in the shoulder and elbow joints, is seven centimetres shorter 
than the right, while the left lower extremity is three centimetres shorter than 
its fellow. The whole half of the body has shared in the atrophy, which is also 
well marked in the nates. The circumference of the left upper arm measures 
four centimetres and a half, that of the left leg three centimetres less than that of 
the corresponding extremity. When the patient was fourteen years old the con- 
vulsions reappeared, and he has still one or two epileptiform attacks a week. 
He is quite demented. 



27 5 DISEASES OF THE BRAIN PROPER. 

signs enough to enable us to differentiate between the two 
affections. A hemiplegia due to cerebral haemorrhage can in 
most cases be excluded, owing to its rarity in childhood. Such, 
moreover, would usually not be associated with any muscular 
atrophy. 




Fig. 85. 



Prognosis. — The prognosis quoad valetudinem is absolutely, 
quoad vitam relatively unfavorable. Complete recovery is im- 
possible, and has never been observed. If the patient does not 
succumb during the first days of the disease, he will remain a 
cripple all his life, his mental condition being good only in the 
most favorable cases. Under unfavorable conditions he may 
be epileptic and weak-minded, and to a greater or lesser extent 
deprived of the use of his limbs. The utmost we can expect is 
that the diseased side may atrophy only to a moderate degree, 



CEREBRAL PALSY OF CHLLDREN. 



277 



that the patient may be sound enough in other respects, bodily 
and mentally, and thus be capable of making his own living 
(Figs. 85 and 86). 

Treatment. — The treatment is, on the whole, entirely un- 
satisfactory. Even by the light ol an early diagnosis we are 




The patient now thirty-four years old, fell, at the age of three, from a high 
foot-stool and injured the right side of his head. He lost a considerable amount 
of blood, and was unconscious for quite a long time. Six months after the in- 
jury the atrophy of the left side of the body became apparent, first in the upper, 
then in the lower extremity. With the exception of this atrophy, which has 
now taken in the whole half of the body, including the thorax (compare the left 
with the right mamma), the patient is perfectly healthy. He has never had epi- 
leptiform attacks, there are no hemiathetoid movements, and no psychical alter- 
ations whatever. 



2 7 8 



DISEASES OF THE BRAIN PROPER. 



not in a position either to prevent the continuance of the epi- 
leptiform attacks or to ward off the changes in the affected 
extremities, the symptoms of irritation, the atrophy, etc. The 





Fig. 87. 
The patient, now eighteen years of age, had, when six months old, an "apo- 
plectic stroke," and never learned how to walk properly, since the left half of the 
body was paralyzed up to her second year. The power of motion has improved 
to a certain extent ; the left leg, however, and the left arm have remained be- 
hind in development, so much so that the arm is eight centimetres, the leg 
twenty-five centimetres shorter than the corresponding limb of the right side. 
The shortening of the leg is partly due to a resection of the knee joint per- 
formed thirteen years ago (the reason for which procedure could not be made 
out). Patient suffers from epileptiform attacks, occurring once a month ; they 
last from a quarter to three quarters of an hour, and consist of more or less vio- 
lent convulsions. During these, consciousness is sometimes completely re- 
tained. There is no trace of dementia. 



CEREBRAL PALSY OF CHILDREN. 



279 



symptomatic treatment of the epileptiform attacks by the dif- 
ferent bromides and the galvanization of the atrophic parts is 
all that lies in our power, and, unfortunately, little enough is 
accomplished by these means. 




Fig. 88. 

The patient is now forty-four years old. The date of onset of the disease 
can not be definitely determined. She suffered from epileptiform convulsions 
from early childhood up to her tenth year; these have now entirely disappeared. 
At times, however, a "tic convulsif" (in the distribution of the left facial) is 
noted. The development of the left half of the body has been retarded, the 
upper extremity being two centimetres, the lower three centimetres shorter than 
the corresponding limb of the right side. There is also a difference of from 
four to five centimetres in the circumference of the limbs of the two sides. 
The shoulder, elbow, and wrist joints are contracted, the first being in a posi- 
tion of adduction, the second in one of flexion, and the third in extension. 
Marked degree of dementia. 



28o 



DISEASES OF THE BRAIN PROPER. 




Fig. 89. 



The patient, who is now twenty-two years of age, was taken ill with con- 
vulsions in early childhood. They ceased, but after an interval of ten years re- 
appeared in his fourteenth year, and have continued up to the present time, 
being quite severe and recurring quite frequently. From childhood he has suf- 
fered from a severe motor speech disturbance, and is only able to utter a few 
unintelligible syllables, and that with great effort ; at such times almost all the 
muscles of the body are affected with associated movements. Atrophy of the 
left side is to be noted. The circumference of the left upper arm measures 
three centimetres, that of the left forearm two centimetres, that of the thigh 
four centimetres, and that of the leg two centimetres less than the correspond- 
ing measurements on the right side. The left arm is one centimetre, the left 
leg one centimetre and a half shorter than the right arm and right leg respect- 
ively. The left hand and fingers are in flexor contraction. Patient is moder- 
ately demented. 



THE A THE TO ID MOVEMENTS. 2 8l 

^Etiology. — Although nothing certain is known about the 
aetiology, it seems highly probable that the disease is of an 
infectious nature. In favor of this idea is the fact that it not 
rarely follows acute infectious diseases, especially scarlet fever. 
It has also been recorded after whooping-cough (Marie, cf. lit.). 
That traumatism may be the causative factor is proved by the 
case represented in Fig. 86. The patient at the age of three fell 
head first from a chair and injured himself in the right parietal 
region by striking against a sharp object. If the traumatism 
occur during intra-uterine life or soon after birth, the skull may 
become asymmetrical and the affected side often remain behind 
in development. Syphilis also deserves a place in the aetiology 
of infantile cerebral paralysis. 

" Athetosis." — It remains now for us to describe those 
peculiar involuntary movements above referred to which are 
known to follow cerebral infantile paralysis. The patients are 
absolutely unable to keep the fingers and the toes of the affect- 
ed side still ; they are in constant motion day and night, dur- 
ing waking and sleeping, without interruption. If we observe 
these movements more closely, we find them to be relatively 
slow, rhythmical, and monotonous. The fingers seem to be 
directed with a definite aim, as if they were attempting to seize 
something, and it is easily remarked that the normal limits of 
the movements are exceeded — the fingers are hyper-extended, 
the toes are elevated almost at right angles or fasten them- 
selves to the floor like claws, etc. (cf. Fig. 92). All this is only 
possible in consequence of an unusual stretching of the liga- 
ments, which also admits of positions of distinct subluxation. 
The will of the patient has hardly any influence over these 
movements, and only in light cases, and then but temporarily, 
may the patient succeed, by firm pressure of the affected hand 
upon the body, or by fixing the fingers with the unaffected 
hand, in restricting a little the abnormal excursions ; as soon 
as the mechanical impediment is removed, they will, however, 
begin again with increased vigor. 

The muscles of the forearm present a firmer consistence, a 
certain degree of hypertrophy. The arm feels hard and the 
surface temperature is 0.5 to i° C. (0.9 to i.8° F.) higher than 
on the opposite, sound, side ; not but what the muscular strength 
is materially lessened and sometimes so much diminished that 
the examination with Duchenne's dynamometer yields aston- 
ishing results. With the affected arm the patient can hardly 



282 



DISEASES OF THE BRAIN PROPER. 



lift five kilogrammes, notwithstanding the apparently good de- 
velopment of the muscles, while with the well arm five to eight 
times as much work can easily be done. In the muscles of the 
lower extremity a similar condition may be noted ; not infre- 
quently the ankle joint takes part in these movements of the 





I 



Fig. 90. 



toes, and, in exceptional cases, the knee-joint as well. Other 
muscles than those of the extremities are not affected. 

The first who studied these movements carefully was Ham- 
mond, of New York, in 1871. He gave them the special name 
athetosis (cl-tlOtj/m) and raised them thus to the dignity of a sepa- 
rate disease, which, in our opinion, they never deserve. Athe- 
tosis — and by this we mean the athetoid spasms — does not con- 



THE A THE TO ID MOVEMENTS. 



283 



stitute a disease, but merely a symptom. It is the expression 
of cerebral affections, the anatomical basis of which is variable. 
Only in the rarest instances, one could almost say never, do 
athetoid movements occur alone without any other symptoms. 
Almost always they are associated with other disturbances, 
either psychical (the patients are mentally undeveloped, de- 




Fig. 91. 

The onset of the disease can not definitely be fixed, since the mother of 
the patient does not remember it, and the patient herself, who is now eighteen 
years old, is demented and completely deprived of the power of speech. The 
fact, however, that the illness began in early childhood with convulsions is un- 
questioned ; it is, however, not known how long they lasted nor what followed 
them. When the girl was five years old she was not yet able to walk, because 
the left leg was moved only with difficulty, and the foot gradually assumed an 
equino-varus position, which can still be noted. Patient now walks on the 
outer edge of her foot, and the leg is scarcely moved at the knee joint. The 
left upper extremity can be moved voluntarily in the shoulder and elbow joints ; 
the fingers and the hand present athetoid movements, while in the facial mus- 
cles of the left side a marked " tic co7ivnlsif " is noted. Marked dribbling of 
saliva. Patient no longer suffers from epileptic attacks, but has from time to 
time periods of excitement, during which she becomes aggressive. 



284 



DISEASES OF THE BRAIN PROPER. 



mented, sometimes of a changeable, irritable disposition) or 
somatic, such as paralyses or spasms in the distribution of 
different nerves — for instance, the facial — or contractures, etc. 
Again, the patient may be subject to epileptiform attacks 
which recur at intervals of various lengths. 

If we thus affirm that every athetosis — be it the much rarer 
bilateral form (cf. the case of Bourneville and Pilliet, lit.), be it 
unilateral, the " hemiathetosis " — is only to be regarded as a 
symptom, we are, on the other hand, willing to admit that 
there are individual cases where the athetoid movements are 
such a prominent and dominating feature of the case that we 
may overlook others, or at least not be inclined to attribute 
any importance to them. So it is in an instance reported by 
Gnauck, who speaks of a primary — that is, idiopathic — atheto- 
sis, but who has noted a simultaneous paresis of the facial and a 
hemianaesthesia of the affected side. We can hardly call this 
an idiopathic affection, but must rather look upon it as a pre- 
hemiplegic phenomenon (cf. page 220) ; and, similarly, some 
explanation can be found for the few remaining cases published 
as " idiopathic " athetoses, some of which were congenital. 
These movements are always a symptom of cerebral disease. 
That they are occasionally met with in the course of other dis- 
eases — e. g., spinal affections, especially tabes — there can be no 
doubt. What is the pathological nature of the brain disease 
which gives rise to these spasms is still hypothetical. There 
are cases where no lesion at all was found at the autopsy. One 
thing, however, we know for certain, namely, that these move- 
ments may occur in different cerebral lesions — that is, that 
they constitute a symptom which is not confined to one par- 
ticular disease, but is common to several. Among these, cere- 
bral infantile paralysis, with the anatomical changes described 
on page 268, deserves the first place. Here athetosis (always 
only hemiathetosis) is relatively frequent, and here we have 
the best opportunity for studying its peculiarities. It has also 
been observed in connection with small foci of softening in 
the basal ganglia, the thalamus (Lauenstein), the corpus stri- 
atum (Schulz), and in the temporal lobes (Ewald), although we 
can in none of these instances be certain that the lesions found 
were actually the cause of the movements. After cerebral 
haemorrhage where we have a lesion of the internal capsule, 
in old hemiplegias therefore, hemiathetoid movements are oc- 
casionally seen, yet, in comparison with the frequency of cere- 



THE A THE TO ID MOVEMENTS. 



285 

bral hemiplegias in adults, these are very rare, certainly much 
rarer than in the so-called infantile hemiplegias. We see, there- 
fore, that cortical lesions and lesions of the cortico-muscular 




Fig. 92. 

The patient, now twenty-nine years old, was taken at the age of six months 
with an " apoplectic stroke " followed by convulsions, which at first occurred 
at long intervals, later more frequently, viz., about once every two weeks ; they 
presented all the characteristics of epileptiform seizures. Quite early, peculiar 
involuntary movements appeared in the left extremities, more particularly in 
the left arm, which must be considered as athetoid. At regular intervals the 
fingers are extended and again drawn into the hollow of the hand, this being re- 
peated about fifty times a minute. In the left foot similar, although, of course, 
less pronounced movements, occurring especially in the ankle joint, are noted. 
At about the age of five the convulsions reappeared, although occurring with 
diminished frequency, i. e., from three to five times a year. The patient is ex- 
citable, irascible, and at times even violent. Intelligence is normal. 



286 DISEASES OF THE BRAIN PROPER. 

tract as well as of the basal ganglia may give rise to athetoid 
movements, although we do not understand the nexus cansalis, 
if indeed such exist. In our opinion, disease of the cortex un- 
doubtedly plays the principal part in the causation of athetosis, 
and we can all the more reckon upon the occurrence of athe- 
toid movements if the cortical disease has appeared in early 
childhood and has been either entirely confined to or has af- 
fected more particularly the motor region, the central convo- 
lutions, and the adjacent portions. In lesions of the other 
parts of the brain, especially of the basal ganglia, the thalamus, 
the lenticular nucleus, and the caudate nucleus, athetoid move- 
ments are only exceptionally developed, the conditions which 
favor their occurrence being then wholly unknown. That 
there is a cerebral lesion which produces no other symptom, 
whether psychical or somatic, than these movements is un- 
likely, and consequently, as we said, the name " athetosis," as 
indicating a separate disease, can not be held to be justifiable. 

If one keeps, then, the characteristics of the movements 
which have just been described well in mind, and especially if 
one has had occasion to study their peculiarities, one can hardly 
mistake them for anything else. A good point to remember is 
that they continue during sleep, so that the patients have to 
stop or at least impede them by mechanical appliances. 

We shall give up the idea of chorea or hemichorea which 
we might entertain should the athetoid movements be accom- 
panied by facial spasm, if after observation of the patient we 
have been convinced that the movements persist when the 
patient is asleep. Furthermore, the duration of the disease and 
the fact that it resists all therapeutic measures, more especially 
the protracted use of arsenic, are facts not reconcilable with 
the diagnosis of chorea. Other points of difference will be 
found in the chapter on the latter disease. 

We can not speak of an aetiology of the affection, because, 
as we have said, athetosis is not an affection in itself, and the 
setiological data therefore to be considered are those of the es- 
sential disease upon which the athetoid movements depend. 

We possess no specific which will put a stop to these athe- 
toid movements ; their treatment is that of the primary dis- 
ease, and, as this is usually beyond our reach, the outlook in 
athetosis is necessarily very gloomy. If Hammond claims to 
have effected a cure by stretching the median nerve, we may 
be pardoned for asking how long this cure lasted, and if 



THE A THE TO ID MOVEMENTS. 287 

Gnauck has seen the movements disappear after the use of the 
galvanic current and the internal administration of potassium 
bromide, we are justified in assuming that in his case the affec- 
tion was due to a functional disturbance of the motor area. 
What lasting good results can be accomplished by lryoscine, a 
drug which has been used by Erb, I have not been as yet able 
to establish with the material at my disposal. 

LITERATURE. 

Cotard. Etude sur l'atrophie partielle du cerveau. Paris, 1868. 

Hadden. An Anomalous Case of Infantile Hemiplegia. British Med. Journal, 

February, 1882. 
Wuillamier. De l'epilepsie dans l'hemiplegie spasmodique infantile. These de 

Paris, 1882. 
Jensen. Ein Fall von Entwicklungshemmung in der motorischen Sphare des 

Grosshirns. Arch. f. Psych., xiv, 3, 752, 1883. 
Hadden. On Infantile Spastic Paralysis. Brain, p. 302, 1883, 1884. 
Gaudard. Contribution a l'etude de l'hemiplegie cerebrale infantile. Diss, inaug. 

Geneve, 1884. 
Striimpell. Ueber die acute Encephalitis der Kinder. Polioencephalitis acuta, 

cerebrale Kinderlahmung. Vortrag, gehalten auf der 57. deutschen Natur- 

forscher-Versammlung zu Magdeburg. 
Jendrassik et Marie. Contribution a l'etude de l'hemiatrophie cerebrale par 

sclerose lobaire. Arch, de Physiol., i, 1885. 
Richardiere. Etude sur les scleroses encephaliques primitives de l'enfance, 

Havre, 1885. 
Marie. Hemiplegie cerebrale infantile et maladies infectieuses. Progr. med., 

xiii, 2me ser., No. 36, 1885. 
Bernhardt, M. Ueber die spastische Cerebralparalyse im Kindesalter. Vir- 

chow's Arch., Bd. cii, 1885. 
Bernhardt. Jahrbuch f. Kinderheilk., N. F., xxiv, p. 384, 1886. 
Kast. Zur Anatomie der cerebralen Kinderlahmung. Arch, fiir Psych., xviii, 

2, 1887. 
Mathieu. Progr. med., 2, p. 29, 1888. (Cerebral infantile paralysis as a conse- 
quence of traumatism.) 
Wallenberg. Veranderungen der nervosen Centralorgane in einem Falle von 

cerebraler Kinderlahmung. Arch. f. Psych., xix, 2, 1888. 

Athetosis. 
Shaw. St. Bartholomew's Hospital Reports, ix, 130, 1873. 
Berger. Article on " Athetose " in Eulenburg's Real-Encyclopadie der gesamm- 

ten Heilkunde, ii. Auflage. 
Oulmont. Etude clinique sur l'Athetose. Paris : Delahaye, 1878. 
Leube. Deutsches Arch. f. klin. Med., xxv, 1880. 
Bidon. Essai sur l'hemichoree symptomatique des maladies de 1'encephale. 

Revue de med., 1886. 
Bourneville et Pilliet. Deux cas d'athetose double avec imbecillite. Arch, de 

Neurol., xiv, No. 42, 1887. 



288 



DISEASES OF THE BRAIN PROPER. 



Gerling. Ueber Athetosis. Inaug. Diss. Kiel, 1887. 

Rubino. Contribuzione clinica alio studio dell' atetosi e del paramioclono molte- 

plice. Riforma medica, 258, 1887. 
(Cf. besides the text-books of Striimpell, Seeligmialler, Eichhorst.) 

BRAIN TUMORS. 

Pathological Anatomy. — Brain tumors may be either sharp- 
ly circumscribed or diffuse, in the latter case taking the place, 
as it were, of the brain substance proper. The most common 
— e. g., the gliomata, the carcinomata, and the sarcomata — 




Fig. 93- — Glioma Telangiectaticum. (After Ziegler.) Frontal section through the 
brain, a, right centrum semiovale. b, glioma in the left hemisphere. 



occur in both varieties. The clinical manifestations of brain 
tumors depend upon the rapidity of their growth ; this, 
again, upon their anatomical nature. Among the most im- 
portant and the most frequent forms of tumors must be men- 
tioned : 

The glioma, a form which is peculiar to the central nervous 
system, but is found much more frequently in the cerebrum 
than in the brain stem or the spinal cord. It is formed by 
an increase in the cells of the neuroglia, the axis cylinders 
in the involved region first becoming swollen, and the nerve 
fibres then destroyed. If the newly formed cells are small 
and comparatively few in number, and if their fibrilla-like 
processes form a dense net-work, then the tissue of the growth 



BRAIN TUMORS. 



289 



is firm and solid ; if the cells are numerous the tissue is softer. 
On section, the glioma looks gray, grayish-red, or yellowish, 
sometimes variegated, and if, as is not uncommonly the case, 
it contain areas of hemorrhagic softening, the tumor may be 
filled with opaque more or less fluid masses. The diameter 
of a glioma may measure from three to eight centimetres. 
The transition into the adjoining substance of the brain may 
be gradual or abrupt, and the tumor appear macroscopically 
sharply defined. The affected part of the brain is enlarged, 
but keeps its normal configuration while the ventricles are 
often dilated (Fig. 93). 

The tumor nearest related in texture to the glioma is the 
sarcoma ; it occurs in soft nodes, which, on section, present a 
marrowy, grayish-white appearance. It is seen much more 




Fig. 94.— Papillary Carcinoma in the Third Ventricle. (After Ziegler.) Frontal 
section through the brain. «, tumor with cysts, b, right thalamus, c, lenticular nucleus. 
d, internal capsule, e, caudate nucleus. /, left thalamus, g, lenticular nucleus, h, in- 
ternal capsule, z', dilated lateral ventricle. 



frequently at the base than at the convexity of the brain, and 
not uncommonly is found to originate from the dura, from the 
periosteum of the skull bones, or from the skull itself (osteo- 
sarcoma). According to the character of the cells, we distin- 
guish a round-cell sarcoma, a spindle-cell sarcoma, a fibro- 
sarcoma, etc. In size they may vary from that of a walnut 
to that of a man's fist, and may be solitary or multiple. 

*9 



290 DISEASES OF THE BRAIN PROPER. 

The carcinoma, which appears usually in the brain as 
secondary to carcinoma of the breast, lung, or pleura, is found 
especially in the ventricles as a soft tumor (cf. Fig. 94), dis- 
placing the neighboring brain substance, and giving rise to 
hydrops ventriculorum. 

Clinically of great importance are the tubercles and the 
syphilomata (gummata), which, although they strow macro- 
scopically as well as histologically much similarity, can with 
certainty be distinguished by the presence or absence of the 
tubercle bacilli. They also may be either sharply defined or 
infiltrate the tissue ; they appear on section as yellowish, 
cheesy tumors consisting in part of granulation tissue. The 
" solitary tubercles," which may reach the size of a hazelnut, 
are single or multiple ; they occur by preference in the pons, 
in the cerebellum, and in the cortex. Syphilomata more fre- 
quently originate in the dura mater, and thence invade the 
brain substance. 

The psammomata, which, coming also from the dura, are 
characterized by calcareous concretions imbedded in them ; the 
cholesteatomata, which on section have a lustre like that of 
mother-of-pearl ; the lipomata, often found in the corpus callo- 
sum ; the enchondromata, which originate especially from the 
bones of the base — all these are clinically of little importance, as 
they produce, owing to their relatively small size, either only 
insignificant or no symptoms at all. Hence we may well omit 
them in our description. 

At the autopsy we can often demonstrate the consecutive 
changes produced by a general compression of the brain. The 
skull bones themselves in young people may appear perforated 
and riddled with holes, there may be gaps in the dura or signs 
of inflammatory irritation, certain areas may be rough and 
thickened, presenting a velvety appearance, the convolutions, 
flattened and pressed against each other, have lost their dis- 
tinctness, the pia looks dry and anaemic. Certain alterations 
of shape seem always to occur if the pressure reaches a con- 
siderable degree ; thus a pressure in one hemisphere exerting 
itself from above downward changes more especially the shape 
of the insula and the portions of the temporal and parietal lobes 
which cover it in (Wernicke). This effect must be attributed 
not only to the increase in volume of the tumor, but also to the 
increased amount of the fluid in the ventricles, the hydrops 
ventriculorum (internal hydrocephalus) which almost con- 



BRAIN TUMORS. 29 1 

stantly accompanies tumors. No doubt this internal hydro- 
cephalus itself is due to pressure on the venous trunks in the 
brain, and it occurs, therefore, earlier, and is more marked if 
the large venous trunks coming from the tela choroidea are 
pressed upon by the tumor (Wernicke). 

On the cranial nerves signs of pressure have also been 
noted. The optic tract, the oculo-motorius, the abducens 
(Turck) have been found compressed by tightly stretched 
vessels, and an exudation into the sheath of the optic nerve 
has been observed (Leber). In some cases we find a more or 
less widely spread softening in the parts surrounding the 
tumor, in others this may be entirely absent ; if the softening 
is of a hasmorrhagic character, this must be attributed to a 
cutting off of the arterial blood supply produced by the cere- 
bral compression and to venous stasis. Sometimes, in the 
neighboring vessels, there develops an arteriitis obliterans with 
its sequelae (C. Friedlander). Cranial nerves in the immediate 
neighborhood of carcinomata and syphilomata are found to be 
infiltrated with the tumor elements (Wernicke). 

./Etiology. — The aetiology of brain tumors is entirely ob- 
scure : we do not know in the least whether certain external 
influences increase the predisposition to tumors in the brain or 
not, just as we are entirely ignorant of the aetiology of tumors 
in general. Although the common idea exists that traumatism 
may be the starting point for a new growth, it is difficult to 
understand the connection ; certainly, however, this factor 
plays an infinitely smaller part in tumor than in brain abscess, 
and the occurrence of a brain tumor following an injury is 
probably for the most part accidental. No doubt, in some 
kinds, hereditary predisposition must not be disregarded, as 
in carcinomata and tubercles, but even this loses some of its 
significance, because malignant brain tumors, especially car- 
cinomata, are usually secondary, as we have said. Nothing 
remains, then, but to inquire how far age and sex influence 
their occurrence. With reference to the former, it is supposed 
that some brain tumors, such as tubercles, predominate in the 
young, while carcinomata and sarcomata are chiefly found in 
older people ; others — e. g., myxomata and sometimes gliomata 
— are congenital (Virchow). As to sex, older and more recent 
authors (Lebert, Friedreich, Hasse) agree that males are more 
liable to brain tumors than females, and Wernicke has calcu- 
lated that the proportion is about three to two. 



292 



DISEASES OF THE BRAIN PROPER. 



Symptoms. — The symptoms we are wont to observe in 
brain tumors are due to the mechanical influence which the 
tumor exerts by general or local compression of the skull con- 
tents, and, further, to destructive or irritative actions which 
depend upon certain vital peculiarities of the growth, the 
irritation mostly accompanying the infective neoplasms. One 
or the other of these just-mentioned factors will influence the 
clinical picture of the disease in a more or less characteristic 
manner, and as one or the other is more prominent the whole 
aspect of the disease will vary. 

With reference to the former, the increased intracranial 
pressure, if it appears acutely, we have first a displacement, 
then an increase of tension in the cerebro-spinal fluid. In 
chronic processes the latter does not necessarily occur, but as 
the skull cavity gradually becomes encroached upon, some of 
the fluid ma}' be absorbed or the brain become atrophic. As 
the intracranial pressure becomes higher the circulation in the 
brain and its membranes is retarded. What is the cause of 
this retardation, whether the diminution in the tone of the 
vessel walls produces such an increase in the tension of the 
cerebro-spinal fluid that by compression a narrowing in the 
capillaries is produced or whether fluxionary hyperasmias come 
into play, we are not able to decide definitely. At any rate, if 
the blood current in the interior of the skull frequently under- 
goes a slowing, there is a tendency to increased transudation 
and lymph formation, and with it a danger of oedema of the 
brain (cf. von Bergmann, Die Lehre der Kopfverletzungen, 
Stuttgart, 1880, pages 316-364). 

The symptoms to which this increase of the intracranial 
tension gives rise, and which one has frequently the oppor- 
tunity of studying in the course of brain tumors, may be di- 
vided into general and focal. The former, for the knowledge 
of which we have to thank especially Leyden, Manz, and 
Duret, usually appear in a regular sequence and are always 
the same for the same degree of pressure. 

The most conspicuous and earliest to appear is the head- 
ache. The patient complains of nothing but his head, which 
feels heavy and dull. Every movement causes pain, and this 
becomes at times so violent that the patient feels as if he were 
losing his reason. The pain seems diffuse and can not be local- 
ized. It is in front on the forehead, behind over the occiput, 
to the right, to the left; it torments him everywhere, and the 



BRAIN TUMORS. 



293 



lightest tap with the finger anywhere upon his head is intensely 
disagreeable. Sometimes there comes an hour or two of relief, 
although the patient feels by no means well and is never with- 
out pain even in sleep. The seat of this pain, which is due to 
the general increase of the intracranial pressure produced by 
the tumor, is not known. It is, however, not likely to be in 
the substance of the brain itself, unless it be perhaps in the 
corpora quadrigemina and the thalami. We should rather 
look for its position in the dura, which derives its nerve supply 
from the trigeminus (cf. page 3). If the fibres of this nerve 
are compressed by the tumor in the posterior fossa, then there 
is not the vague pain taking in the whole head, but another 
well-defined headache referred by the patient to the back of 
the head and neck only, a trigeminal or occipital neuralgia 
which is not a general but a focal symptom. This double sig- 
nificance of the headache may become a very valuable point 
in the topical diagnosis. Entire absence of headache is rare, 
and we are only without this symptom when the growth of 
the neoplasm is slow. Its occurrence with unwonted vehe- 
mence has repeatedly been noted in aneurisms situated near 
the dura. Occasionally it disappears when definite focal symp- 
toms become established, and it becomes more obscured in the 
later stages of the disease, when the patient becomes somno- 
lent. Its existence is then only apparent from the fact that 
the half-unconscious sufferer frequently puts his hand to his 
head and moans. 

A second general symptom is afforded by the epileptiform 
convulsions, which either affect the whole body or are confined 
to one side and during which consciousness may or may not 
be completely lost. They are by no means so frequently asso- 
ciated with brain tumors as headache, still their occurrence is 
common enough to be of diagnostic value. They, too, may 
constitute a focal symptom, as is, for instance, not rarely the 
case in cortical tumors of the frontal or parietal lobes, which, 
partly, exert local pressure, partly, irritate the cortex. We 
must not suppose that these two symptoms, although they are 
both of an irritative nature, always go hand in hand. Either 
one or both may be present, sometimes the one as a general, 
the other as a focal symptom. Convulsions occur in about 
fifty per cent of all cases of brain tumors. 

The psychical changes constitute a third general symptom, 
which, however, disturbs less the patient himself than his 



! 9 4 



DISEASES OF THE BRAIN PROPER. 



friends. A certain slowness in thinking- is occasionally noticed 
in the patient, at first temporary, but later more constant — an 
inability to appreciate properly the commonest details of daily 
life which had never been before remarked in him. At the 
same time the features become dull and lose their animated ex- 
pression, his movements become slow and awkward, he grows 
careless in ail his doings, and this listlessness about everything 
going on around him may be carried to such an extent that he 
lets his urine and faeces pass from him, without showing any 
concern, or attempting to satisfy his needs in a proper manner. 
Gradually he begins to show occasional signs of bewilderment. 
Things that he meets with every day he no longer recognizes. 
His own house seems strange to him, he forgets the way to 
his dining and bed room and has to be shown there, etc. 
He even forgets how to read and to write, how to solve the 
simplest mathematical problems which would not give the 
slightest difficulty to an eight-year-old child, and gradually he 
becomes more and more demented, until this condition passes 
into one of deep coma and death. In other cases the intelli- 
gence seems to remain intact for a long while, and only the 
weakness of memory strikes one. The friends of the patient 
become alarmed on noticing that he forgets things which he 
has said or done only one or two days or even a few hours be- 
fore, that he does not remember the visits of the physician 
who comes daily, but complains of not having seen him for a 
long time. Yet although he may be troubled with bodily pain, 
the patient may seem at the same time cheerful, inclined to 
jest, and to look at things from the humorous side, and it is 
not until later that the other mental defects also begin to show 
themselves, and not infrequently the physician is not consulted 
until the friends discover that the patient is no longer capable 
of conducting his own affairs. Actual speech disturbances do 
not usually occur. Certain peculiarities of speech which do 
come on and make it different to that in health are due to the 
extensive loss of memory of the patient, owing to which he has 
difficulty in finding the right expressions, and often mixes 
them up, etc. This makes him uncertain in speaking. He 
talks slowly, and his deliberation becomes quite noticeable. 

In consequence of the increased intracranial pressure, not 
rarely disturbances in the sensorium occur. The patient is in 
a dazed condition, has a constant desire to sleep, and is drowsy. 
The pulse then is often slow at first (forty-five to fifty-five beats 



BRAIN TUMORS. 2 Q$ 

per minute) and irregular, similar to that which we may ob- 
serve in apoplexy. This retardation is finally followed by an 
increase in the frequency in the number of beats. In other 
words, the primary irritation has given way to paralysis of the 
vagus. 

Together with the action of the heart, respiration is affected. 
During coma it is deep, slow, and often stertorous ; with the 
continued increase of the cerebral compression it becomes ir- 
regular and shallow. Deep inspirations are interrupted by 
long pauses, in one of which the patient dies. 

Slight vertigo, sometimes attended with vomiting, is not 
uncommon. The latter, which is cerebral in origin, has certain 
peculiar characteristics. It usually occurs on the slightest 
provocation. It may be provoked by a simple change in the 
position of the body, and often comes on in the early morning 
and without the existence of any stomach trouble. Without 
any retching large amounts of watery clear stomach contents 
are repeatedly thrown up, and after a short while the patient 
feels perfectly well. Sometimes the vomiting is the forerunner 
of apoplectiform attacks, in which the patient may be uncon- 
scious for hours. Such attacks are due to a sudden increase in 
the intracranial pressure, either from haemorrhage into the sub- 
stance of the tumor or from sudden hydrocephalic exudations 
(Wernicke). 

That papillitis is extremely common in brain tumor we 
have said before. We may add here that it may exist without 
headache, for the increase in the intracranial pressure sufficient 
to produce papillitis does not necessarily produce an appre- 
ciable irritation of the dura, and, on the other hand, if head- 
ache exists without papillitis, it is not referable to the cere- 
bral compression but to irritation of the dura. We should 
never forget that papillitis may exist without any visual dis- 
turbance, and hence never omit the ophthalmoscopic examina- 
tion in suspicious cases, no matter whether the patient com- 
plains of trouble with his eyesight or not. Again, the patient 
may only complain of one eye, while the other seems to per- 
form its function normally, and yet profound changes be found 
in either fundus. 

If in the course of a brain tumor the patient develops in 
addition to papillitis an early blindness, then the amaurosis has 
to be interpreted as a focal symptom, and the tumor located in 
the cerebellum, as neoplasms in this situation are usually at- 



296 DISEASES OF THE BR AIM PROPER. 

tended with very marked internal hydrocephalus, especially of 
the third ventricle, the floor of which becomes distended and 
presses upon the chiasm situated under it (Tiirck). Moreover 
early amaurosis may be produced by tumors in the region of 
the corpora quadrigemina, especially those of the pineal gland, 
by basal neoplasms, which, just as those of the pituitary body, 
press on the chiasm and the beginning of the optic tract, or 
which raise the base of the brain from the base of the skull, 
so that the artery of the corpus callosum is made tense and 
compresses the optic nerve (Tiirck). 

In considering the focal symptoms produced by brain 
tumors we must first of all state that these may be entirely 
absent, just as we have seen is sometimes the case in brain 
abscess. Instances of this kind have repeatedly come under 
observation, and it was on this very account found impossible 
to make a certain diagnosis during life. Absence of both gen- 
eral and focal symptoms is very rare, and only possible when 
the new growth is very limited, and situated at an indifferent 
place. Further, there are symptoms which we are justified in 
taking for focal symptoms, but which are in reality due to the 
general compression. The most important of this nature is 
hemiplegia. We may in a case of brain tumor find a well- 
marked hemiplegia, which persists without any amelioration, 
and be induced to call it a focal symptom, and yet, to our sur- 
prise, at the autopsy a tumor may be found in an entirely in- 
different area — for instance, in the white matter of the frontal 
lobes — a connection which we could not reckon upon. An in- 
stance of this nature I had published in an inaugural disserta- 
tion. This was the case of a man fifty years of age who suffered 
from mitral insufficiency, and who was seized with a grave 
right-sided hemiplegia which persisted unchanged for months, 
associated with speech disturbances. Papillitis could never be 
demonstrated. The case was then supposed to be one of em- 
bolism in the left middle cerebral artery, but at the autopsy a 
round-cell sarcoma the size of a walnut was found in the white 
matter of the frontal lobe, in the pars frontalis media of the left 
hemisphere (Steinberg, Beitrag zur Localisation der Hirntu- 
moren. Inaugural dissertation. Breslau, 1886). For the hemi- 
plegia to be uncrossed — that is, to be situated on the same side 
as the tumor — is certainly very exceptional ; in our case it was 
crossed. If focal symptoms make their appearance compara- 
tively early we mostly have to do with basal tumors which 



BRAIN TUMORS. 



297 



produce fatty degeneration and gray atrophy of the involved 
cranial nerves, notwithstanding the no inconsiderable power 
of resistance which such nerves possess. Besides the optic 
(unilateral papillitis) and the oculo-motor (ptosis), the fifth, the 
facial, the abducens, and the hypoglossus are then relatively 
frequently affected. Of the fifth, usually only the sensory por- 
tion is implicated ; sensory disturbances in the face, tic dou- 
loureux, later anaesthesia in its area of distribution, occur 
much more frequently than paralysis of the muscles of masti- 
cation. The facial is, on the contrary, affected in its whole dis- 
tribution, a fact which, in conjunction with the reaction of 
degeneration in the paralyzed muscles which also exists, is 
characteristic of the peripheral origin of the paralysis (cf. page 
89). The whole hypoglossus is involved, which causes not 
only the tongue to be protruded to one side, but also leads 
to atrophy in the affected muscles ; swallowing, mastication, 
and speech, are necessarily affected by this. The hypoglossus 
paralysis, however, is much rarer than that of the facial. Com- 
bined affections are found : 

(a) Of the olfactory, the optic, the oculo-motor, and the 
first branch of the fifth in tumors of the anterior fossa. 

(b) Of the chiasm, the oculo-motor, the first branch of the 
fifth, and the abducens in tumors of the pituitary body. 

(<:) Of the oculo-motor, the patheticus, the chiasm, in tumors 
of the middle fossa, if situated above the dura, of the three 
ocular nerves and the quintus, if situated below the dura ; and 
finally, 

(d) Of the facial, the trigeminus, the auditory, the glosso- 
pharyngeal, the vagus, the accessorius, and the abducens in 
tumors of the posterior fossa. 

Diagnosis. — It is the object of our diagnosis in a given case 
to determine first the presence, then the position, and finally 
the nature of a tumor. The first question can, as is apparent 
from what has been said, by no means always be answered 
with certainty ; especially is this difficult if either only general 
or only focal symptoms are present. Among the former, head- 
ache, we have said, plays the most important role. It may last 
for years without any other signs to lead us to suspect a tumor, 
and it is in such instances that we can easily understand how 
this may be mistaken for simple habitual headache or hemi- 
crania, where the pain may also attain an almost unbearable 
intensity. Yet in hemicrania and its allied affections there 



298 



DISEASES OF THE BRAIN PROPER. 



occur remissions, and there are considerable periods of time 
during which the patient is perfectly free from pain ; whereas 
in the course of a brain tumor this never happens. Here we 
find no intervals of relief, but the patient's sufferings are unin- 
terrupted. Moreover a headache, no matter how severe it be, 
which is materially improved by the exhibition of salicylates, 
bromide, or caffeine, etc., we can hardly refer to a serious 
organic brain disease. If, however, it persists uninfluenced by 
all the ordinary therapeutic measures, this ought to put us on 
our guard, and make us look further for focal symptoms — 
unilateral papillitis, for instance — which may be present; yet 
we should, on the other hand, not lose sight of the fact that 
there are quite a considerable number of cases of pure migraine 
which do not yield to remedies, and which have to be regarded 
as incurable. 

Convulsions, although less often than headache, may be the 
only striking symptom. If they last for months, appearing at 
moderately long intervals, we may, in the absence of any other 
symptoms pointing to a tumor, think of idiopathic epilepsy. 
Here, also, the therapeutic test may throw light upon the 
subject. Large doses of bromide usually diminish the fre- 
quency as well as the severity of epileptic attacks, at least for 
a time, and the favorable influence of the drug is often, indeed, 
quite striking, while if the seizures are due to an organic cere- 
bral lesion, bromides, even if they be continued for a length- 
ened period, have but little effect. Such fruitless trials should 
direct our attention again to the possible existence of a tumor, 
and lead us to search for further symptoms which may help 
the diagnosis. 

If the patient complains of nothing further than attacks of 
vertigo and vomiting, if psychical changes, headache, and con- 
vulsions, are absent, then the diagnosis remains uncertain, 
because vertigo can be produced by many different causes, and 
cerebral vomiting is met with in affections so different from 
one another that it is simply impossible to diagnosticate a brain 
tumor from these two symptoms alone. They even do not 
necessarily indicate a brain disease, as we may have to deal 
with Meniere's complication of symptoms, with a stomach- 
neurosis, or a spinal disease — e. g., tabes. The gastric crises 
of the tabetics may resemble very closely the attacks of vomit- 
ing in the course of a brain tumor. 

Among the organic diseases of the brain which may be mis- 



BRAIN TUMORS. 



2 99 



taken for a new growth are brain abscess and meningitis. The 
former — the abscess — is almost always associated with febrile 
movements, and rarely with papillitis; moreover, there are the 
characteristic remissions, so that the patient's general condition 
may be excellent for years. If we keep these points in mind, 
and if we make it a rule never to diagnosticate a brain abscess 
unless we can obtain in the history some astiological datum, 
such as an otitis media, traumatism, etc., the differential diag- 
nosis will usually present little difficulty. In meningitis fever 
is the most important symptom. Papillitis is more frequent 
here than in abscess, and hence of less value in the differential 
diagnosis between tumor and meningitis, yet the early delirium 
and the jactitations are sufficiently characteristic symptoms to 
be of diagnostic value. 

Other diseases to be considered are chronic cerebral sclero- 
sis associated with arterial disease, and lobar sclerosis. The 
absence of grave general symptoms, the usually much slower 
course, the appearance of multiple sclerotic foci, the absence 
of papillitis, are often points enough on which to base a diag- 
nosis. 

Finally, the possibility of confusing brain tumor with pro- 
gressive paralysis of the insane (dementia paralytica) and with 
chronic alcoholism ought to be spoken of. This can, of course, 
only -happen in those cases of brain tumor where apoplectiform 
attacks occur, where headache is either absent or only slight, 
where, however, the mental disturbances are marked, and 
where, owing to the defective memory, the alterations in 
speech become a prominent feature of the case. The course 
will clear up all doubtful cases. If we are dealing with a 
dementia paralytica we shall not have to wait long for the 
appearance of the characteristic delusions of grandeur, and the 
patient will become bewildered and have transitory periods of 
excitement, whereas, with the tumor, stupor and somnolence 
are developed. In chronic alcoholism tremor and the occur- 
rence of stomach and liver affections are usual. Above all, a 
conscientious use of the history will guard us from an error in 
the diagnosis. 

The seat of the tumor we can only attempt to determine 
when we have reliable focal symptoms to aid us, but, as we 
have observed, such may be absent, and, as it seems, this is 
more especially the case in soft tumors occurring in the ventri- 
cles and sometimes in the frontal lobes, which give rise to 



300 



DISEASES OF THE BRAIN PROPER. 



symptoms of general compression only. It is furthermore per- 
fectly certain that a great part of the basal ganglia, the lenticu- 
lar and the caudate nucleus, also the anterior portion of the 
thalamus, the corpus callosum, the fornix, the choroid plexus, 
and finally the cerebellum, with the exception of the vermiform 
process, may be the seat of neoplasms with a complete absence 
of all focal symptoms. On the other hand, tumors of the motor 
area, of the occipital and temporal lobes, of the pulvinar, of the 
crus, the pons, the medulla oblongata, and of the vermiform 
process of the cerebellum, often manifest themselves clinically 
by characteristic focal symptoms, which we here need not de- 
scribe, as they have been considered above in detail. Suffice it 
only to add that destruction of the pulvinar, no less than de- 
struction of the occipital lobe, may give rise to hemianopia, 
that an early oculo-motor paralysis points to the existence of a 
tumor in the crus, while severe general symptoms — tonic con- 
vulsions, without the loss of consciousness, staggering gait — 
indicate a neoplasm in the vermis of the cerebellum. Tumors 
of the medulla oblongata may, if general symptoms are absent, 
simulate bulbar paralysis in their course. Vertigo has often 
been noted in connection with such tumors. Other symptoms 
are changeable and uncertain ; sometimes, indeed, there are no 
symptoms at all. Paralysis of the abducens points to the pos- 
terior fossa as the seat of the neoplasm. The affections of 
other nerves, which are important in this connection, have 
been mentioned above. 

Where we have amaurosis, the pupillary reaction to light 
ought to be carefully examined. Its presence denotes that the 
optic nerve and tract are intact and the new growth can only 
be situated in the central optic fibres, while if it is absent or 
much diminished we have to deal with a lesion of the optic 
nerve or tract. Even with the existence of papillitis the pupil- 
lary reaction may be present. Then the occurrence of the 
former with the central lesion must be considered as an acci- 
dental coincidence. If we think it possible that the amaurosis 
is due to double hemianopia, we may examine for the so-called 
hemianopic pupillary reaction (described on page 34) to throw 
light upon the question. 

The existence of focal symptoms, however, does not always 
facilitate the diagnosis as much as we might suppose. This is 
especially true if the general symptoms are very grave and 
pronounced. As we have remarked, a hemiplegia must not 



BRAIN TUMORS. 



301 



always be taken for a focal symptom, and we must again insist 
that its presence is of no value for the topical diagnosis. We 
need not mention that various disturbances may be produced 
by indirect action which baffle all attempts at a topical diag- 
nosis (cf. the lecture of Jastrowitz, the reference to which is 
given at the end of the chapter). 

The nature of the tumor can in some cases not be deter- 
mined, while at other times it may be very apparent. The 
course of the disease is of less value in this question than, for 
example, the history of the patient's previous diseases, and the 
fact that certain tumors show preference for certain portions of 
the brain, sometimes also the age of a patient, are likely to 
afford us valuable hints. 

Where syphilis has existed, we have to think of gummata. 
If the family history be one of tuberculosis or carcinoma, brain 
tubercles or secondary carcinoma ought to be considered. A 
chronic cerebral affection in a child, attended with headache 
and convulsions, is strongly suggestive of solitary or of multi- 
ple cerebral tubercles. Tumors of the cortex are more likely 
to be of a syphilitic or tuberculous nature, while those of the 
base are preferably sarcomata ; those of the white matter, the 
centrum ovale, gliomata. 

Prognosis. — The prognosis in brain tumor is generally un- 
favorable, and death within one or two years after the appear- 
ance of the first symptoms may be predicted. Spontaneous 
recovery is unheard of, and improvement as a consequence of 
treatment is very rare and has only been observed in cases of 
gummatous or tuberculous neoplasms. Here it occurs beyond 
question, consequently the prognosis is much less gloomy in 
these than in other tumors. In general the course is, in spite 
of all treatment, steadily progressive. The patient's sufferings 
increase in severity and the agony is only blunted by the dull- 
ing of the sensorium. Death occasionally sets in suddenly, as 
a rule only after a protracted state of marasmus in consequence 
of exhaustion. 

Treatment. — The treatment is in the vast majority of cases 
of no avail. Only in rare instances can we by a systematic 
administration of potassium iodide (5.0 to 8.0 (grs. lxxv to 3 ij) 
daily in hot milk for one and a half to two months) effect a 
noticeable improvement. Whether this is due to the direct 
action of the iodide on the tumor or whether only the sec- 
ondary changes, the softening, the oedema, the accumulation of 



302 



DISEASES OE THE BRAIN PROPER. 



fluid in the ventricles are influenced thereby, we do not know. 
As a matter of fact, however, the improvement does occasion- 
ally occur, and, be it explicitly stated, not only in cases of gum- 
mata, but also in other, malignant, neoplasms. Besides iodide 
of potassium arsenic seems at times to have a beneficial action, 
yet sufficient positive observations are wanting on this point. 

The question of operative interference, if such appear indi- 
cated, involves the same principles which we have set forth in 
connection with operation for abscess, and which ought to 
guide us here also. Symptoms pointing unmistakably to an 
exudation into the ventricles justify trephining and tapping 
of the lateral ventricles for the purpose of lowering the intra- 
cranial pressure. The posterior fossa is always a sort of a 
noli me t anger e (Wernicke). Headache, vertigo, and vomiting 
are to be treated symptomatically. 

LITERATURE. 

Obernier, in Ziemssen's Handbuch der speciellen Pathologie und Therapie. Bd. 

xi, i. Abtheilung. 
Bernhardt. Beitrage zur Symptomatologie und Diagnostik der Hirnge- 

schwulste. Berlin, Hirschwald, 1881. 
Heubner. 3 Falle von Tuberkelgeschwiilsten im Mittel- und Nachhirn. Arch. 

f. Psych, u. Nervenkr., xii, 3, 1881. 
Striimpell. Ein Fall von Gehirntumor mit centraler einseitiger Taubheit. Neu- 
rol. Centralbl., No. 16, 1882. 
Andry, J. Les tumeurs des plexus chorioides. Revue de med., vi, 11, p. 897, 

1886. 
Steinberg. Beitrag zur Localisation der Hirntumoren. Inaug. Diss., Breslau, 

1886. 
Heusser. Virchow's Archiv, Bd. 110, p. 9, 1887. (On tumors of the pituitary 

body.) 
Taubner. Ibid., Bd. no, p. 95, 1887. (On lipoma of the brain.) 
Daly. Brain, xxxviii, p. 234, 1887. (Tumor of the pineal gland.) 
Hutchinson. Ibid., p. 223, 1887. (Neoplasms in both corp. striata.) 
Brieger. Berl. kl. Wochenschr., No. 47, 1887. (Case of sarcoma of the pia.) 
Rossander. Hygeia, xlix, 8, 1887. (Fungus dura? matris.) 
Birdsall. Philad. Med. and Surg. Reporter, Ivi, April 18, 1887. 
Churton. Brit. Med. Journ., May 28, 1887. 

Leclerc. Trois cas de tumeurs intracraniennes. Revue de med., 12, 1887. 
Sokoleff. Gliom des Centralnervensystems. Deutsches Arch. f. kl. Med., Bd. 

45, Heft 4, 5, p. 443, 1887. 
Jastrowitz. Beitrage zur Localisation im Grosshirn und deren praktische Ver- 

vverthung. Berl. kl. Wochenschr., xxiv, 49, 50, 1887. 
Suckling. Lancet, ii, 14, 1887. 

Jackson, Hughlings. Brit. Med. Journ., p. 997, 1887. 
Mills, Charles. Journ. of Nerv. and Ment. Diseases, xiv, ii, 12, 1887. 



PARASITES OF THE BRAIN. 



303 



Schmidt-Rimpler. Arch. f. Augenheilk., xviii, 2, 1887. (Glioma of the pons. 

The author speaks of paralysis of the ocular muscles and the origin of 

choked disks.) 
Schweinitz. Philad. Med. and Surg. Rep., lvii, October, 1887. (Tumor of the 

pituitary body.) 
Rousseau. Encephale, viii, 1, 1888. 



APPENDIX. — PARASITES OF THE BRAIN. 

Among the parasites found in the brain the cysticerci and 
the echinococci are the most important. 

The former — the cysticerci — are found quite frequently at 
the autopsy when their existence during life was not diagnos- 
ticated or even suspected, a proof that they may be present 
without giving rise to any symptoms, or that they may pro- 
duce a clinical picture such as is often due to other causes. 
The cysts, which are rarely single, but mostly multiple, 
amounting as they may to one hundred or more in number, 
have their seat, some in the meninges, some in the substance 
of the brain, in the gray as well as in the white matter; some- 
times they are free in the ventricles. They may be so numer- 
ous that the whole surface of the brain is studded with them. 
Their size may vary from that of a bean to that of a walnut, 
and but rarely exceeds that of the latter. They contain a 
serous fluid. At a place where the cyst-wall is somewhat 
thickened are situated the neck and head, the latter often 
darkly pigmented, and to be recognized on closer examination 
by a crown of hooklets and suckers. The parts surrounding 
the cyst are either perfectly normal or in a state of inflamma- 
tory softening. This latter is found as a rule only when the 
cysticercus is dead and has undergone changes. If the cyst 
sends out diverticula it assumes the form of a bunch of grapes, 
and hence is called cysticercus racemosus (Virchow, Mar- 
chand). It is estimated that the parasites live from three to 
six years. After their death they are changed into calcareous 
concretions, surrounded by a connective-tissue membrane, 
which in their interior contain cholesterine and fat. 

Echinococci are usually found in single solitary vesicles 
on the free surface of the brain or the ventricles. Their yel- 
lowish mucoid contents, surrounded by a cyst-wall and a 
connective-tissue capsule, can break through to the outside, 
and be evacuated through the nose, the ears, etc., and a sort 
of spontaneous recovery take place. 



304 



DISEASES OF THE BRAIN PROPER. 




It is impossible to sketch a clinical picture produced by 
cysticerci in the brain, because this varies, of course, with the 
seat of the cysts. I had occasion in the past few years to ob- 
serve four cases in my clinic, and of these only one was diag- 
nosticated during- life, and this one, not because it presented 
characteristic symptoms, but owing to the history of the 

patient, from which we 
learned that he was in the 
habit of frequently eating 
raw pork. In all four cases 
the patients suffered from 
epileptiform attacks with con- 
vulsions, sometimes with, 
sometimes without loss of 
consciousness. T wo of them 
were in the intervals be- 
tween the attacks tempora- 
rily completely bewildered, 
Fig- 95-— Cysticercus Racemosus. (After and were sometimes for hours 

MARCHAND.) n()t able tQ find their way ^ 

the ward where they were staying, did not recognize their 
fellow-patients — in short, presented conditions which, con- 
sidering the attacks which they were subject to, were 
looked upon as epileptic equivalents. Motor disturbances 
were not observed in any of the cases ; all of them, however, 
complained at times of headache and vertigo. In one case 
three cysts the size of a pea were found imbedded in the left 
lenticular and caudate nucleus, the internal capsule being 
spared, and the patient had perfect use of the right extremi- 
ties. In another case there was found a focus of softening the 
size of a pea, in which the calcified remains of a cysticercus 
could be demonstrated, in the left half of the middle segment 
of the pons immediately below the middle line, without there 
having been during life any noticeable symptoms of destruc- 
tion. A third case showed, besides numerous vesicles imbed- 
ded in the gray cortex, cysticerci swimming free in the fluid of 
the ventricles, the amount of which was considerably increased. 
The high grade of hydrocephalus w r as probably responsible for 
the imbecility of the patient, a condition for which during life 
the epileptic attacks had been held accountable ; these, in their 
turn, were doubtlessly connected with the parasites in the cor- 
tex. Cases presenting a course which resembles that of the 



CONGENITAL DISEASES OF THE BRAIN. 



305 



progressive paralysis of the insane I have myself not had occa- 
sion to observe. According to Wernicke such instances are 
not rare (Joe. cit., 11.1, 373). 

The aetiology of cysticerci in the brain is that of cysticerci 
in any other part of the body ; they will develop in persons 
who often give the parasites a chance to invade their body, as 
is, for instance, the case with butchers, and they hence occur 
relatively frequently in such individuals. Therapeutics in this 
case is powerless ; we have no means of destroying the parasite. 

Echinococci of the brain often do not present any peculiar 
symptoms which could be used for diagnosis. The clinical 
picture by which they manifest themselves is usually that of a 
tumor, but when they have perforated to the outside we may 
be able to demonstrate on the protruding tumor fluctuation 
and pulsation. If they perforate into the orbit they give rise 
to oedema of the lids and exophthalmus. Westphal has ob- 
served a case in which over ninety cysts were evacuated to 
the outside. 

That actinomycosis may occur in the human brain is shown 
by the publication of Bollinger (cf. lit.), where a tumor in the 
third ventricle is described which contained numerous char- 
acteristic granules. 

LITERATURE. 

Marchand. Virchow's Arch., Bd. 75. Bresl. arztl. Zeitschr., 1881. 

Zenker. Ueber den Cyst, racem. des Gehirns. Erlangen, 1882. 

Soltmann. Cysticercus cerebri multiplex bei einem ijahr. Kinde. Bresl. arztl. 

Zeitschr., No. 20, 1882. 
Brecke. Ueber Cysticerken im vierten Ventrikel. Inaug. Diss. Berlin, 1886. 
Goldschmidt. Freier Cysticercus im Gehirn. Deutsches Arch. f. klin. Med., 

xl, 3, 4, 1887. (No convulsions.) 
Bollinger. Ueber primare Actinomycosen im Gehirn des Menschen. Munch. 

med. Wochenschr., p. 789, 1887. 
Engel. Ein Fall von Cysticercus beim Menschen als Beitrag zur Diagnostik 

des Cysticercus cerebri. Prager med. Wochenschr., xiii, 2, 1888. 
Gavoy. Cysticerque du cerveau. Encephale, viii, 1, 1888. 

CONGENITAL DISEASES HYDROCEPHALUS MENINGOCELE POREN- 
CEPHALY ABSENCE OF CERTAIN PARTS OF THE BRAIN. 

Our knowledge of the collections of fluid in the brain, 
which are described under the general term of hydrocephalus, 
is, on the whole, very defective, and this is even more true of 
20 



306 



DISEASES OF THE BRAIN PROPER. 



the causes which bring about the abnormal increase. We 
know that the fluid is either contained between the meninges 
or within the ventricles, and speak accordingly of a hydro- 
cephalus externus and internus. We know further that it may 
collect very rapidly or very slowly. In the former case we 
have a hydrocephalus acutus, and in the latter a hydrocephalus 
chronicus. Finally, we know that the conditions under which 
it develops may sometimes exist during intra-uterine life, or, 
again, may appear much later, and we consequently distinguish 
the congenital from the acquired form. But, after all, the dis- 
tinction which we gain by this is only superficial. About the 
exact manner of development of any of these forms there pre- 
vails a great difference of opinion, and the question under what 
circumstances hydrocephalus may develop as an independent 
idiopathic disease can not be satisfactorily answered. There 
is no doubt but that in by far the greater majority of cases we 
have to deal with a congenital disease, and, as a matter of fact, 
this form plays in practice the most important role. 

The congenital hydrocephalus is very rarely external, but 
is much more often internal. It may be well developed at 
birth, so that the circumference of the skull measures sixty or 
seventy centimetres or more. The skull bones then are usually 
so thin that their thickness scarcely amounts to that of a sheet 
of paper. The fontanelles and sutures are separated by wide 
gaps. The distention of the ventricles may be so enormous 
that they form a large cavity which is surrounded by brain 
substance one and a half to two centimetres thick. The lat- 
eral ventricles are usually dilated to a much greater extent 
than the third and fourth ; still, these latter may also be mod- 
erately distended. The whole brain, more particularly the 
basal structures, presents the signs of an increased intracranial 
pressure ; they are flattened out, the commissures are stretched, 
the foramen of Monroe is very large, the walls of the ventricles 
are often covered with granulations, the ependyma inflamed 
and in places slightly thickened. The colorless serous fluid, 
the amount of which may be as much as one and a half litres, 
contains 99 per cent, of water, 0.3 per cent, albumen, traces of 
salts, and so forth, and the sp. gr. is 1.004 to 1.006. 

The most conspicuous symptom of hydrocephalus is the pe- 
culiar enlargement of the head. This is, however, not always 
apparent in the first weeks. Sometimes one and a half or two 
months may pass before the increase in size begins to be notice- 



HYDRO CEP HA L US. 



307 



able. The circumference of the head, which at birth meas- 
ures forty centimetres and a year later forty-four centimetres, 
rapidly becomes greater, and every week a half or one centi- 
metre is added to it, so that after a certain time, often only 
after a few months, the head has reached in circumference a 
size which it does not generally attain to before the age of 
puberty — viz., fifty centimetres. If the distention of the skull 
is equal on all sides it becomes spherical and forms a strik- 
ing contrast to the smallness of the face, which, of course, does 
not take part in the enlargement. If, however, this is more 
marked in the sagittal diameter the skull assumes a dolicho- 
cephalic form, and its appearance is no less bizarre. This is 
still more accentuated by the enormously enlarged veins which 
as blue cords run over the skull. The eyes are frequently di- 
rected downward. This may depend upon an insufficient in- 
nervation of the eye muscles. The appearance of a child with 
a well-developed hydrocephalus, the enormous head, which if 
the child is held erect rolls from side to side, the small trunk 
which with its shrunken limbs looks as if it was only an appen- 
dage of the head, the idiotic facial expression, are together 
characteristic enough to warrant the diagnosis without any 
further examination, which would reveal various motor dis- 
turbances, spasms of the muscles, and sometimes increased re- 
flexes. It need hardly be stated that the intelligence develops 
only in a very imperfect manner or practically not at all. Most 
of the children never learn to speak or at least only imper- 
fectly. They are not able to play like others, their conduct is 
silly and senseless, their habits are dirty, and they require 
much painstaking care and nursing. In exceptional cases their 
mental development reaches a somewhat higher stage and they 
are able to comprehend certain things, so that under particu- 
larly favorable circumstances, as in a well-conducted home for 
feeble-minded children, it may be possible to give such children 
an amount of knowledge and skill which is quite remarkable. 
The appearance of epileptiform attacks, which are always 
to be anticipated, often greatly interferes with such at- 
tempts. 

The course is either chronic or acute. The issue is always 
unfavorable. The children either die during or soon after 
birth or they attain an age of a few months, or finally they 
may live four or five years, while it is very exceptional for 
them to live longer or reach the age of puberty. If, how- 



3 o8 



DISEASES OF THE BRAIN PROPER. 



ever, this happens, the head ceases to grow and remains of the 
same size or becomes even a little smaller and the skull ossifies. 
If death occurs in an earlier stage this happens either during a 
convulsion or comes on gradually as a consequence of general 
marasmus. There is no question but that in face of this affec- 
tion therapeutics is powerless. We may well omit the usual 
inunctions of the skull with mercurial ointment or the painting 
with tincture of iodine, as well as the internal administration 
of iodide of potassium, without any feeling of self-reproach, for, 
often as these measures have been used, rarely has any good 
result from them been seen. Good general nursing of the 
child, later a well-conducted simple instruction as far as this is 
feasible, finally, symptomatic treatment, more especially of the 
more dominating symptoms, as the epileptiform seizures, which 
are best met with bromides, is more rational than any other 
more or less futile measures, not excluding puncture of the 
head and other surgical interference. That we are ignorant of 
the aetiology we have said above, and would only add here 
that the statement, that syphilis and alcoholism in the parents 
are predisposing causes, is without foundation. 

The idiopathic hydrocephalus which appears later in life 
may be connected with atheromatous processes and focal dis- 
eases in the brain. Owing to the rarity of its occurrence, how- 
ever, it has been but little studied, and the possibility that even 
in such cases we have in reality to deal with the secondary, 
deuteropathic, hydrocephalus is by no means excluded. 

The secondary hydrocephalus has at times to be attributed 
to disturbances of the circulation, at times to general disorders 
of nutrition. Among the former may be mentioned active hy- 
peremias of the brain, occurring in consequence of the abuse 
of alcohol, and venous stasis, as it is seen in valvular diseases of 
the heart and emphysema. There are, besides, the circulatory 
disturbances caused by circumscribed meningitides, tumors, 
and abscesses, by which, for example, obstruction of the aque- 
duct of Sylvius may be brought about (Seeligmuller). Among 
the disturbances in nutrition there are certain forms of anae- 
mia, general dropsy, phthisis pulmonalis (Callender). The 
affection may run a very acute course and prove fatal in a few 
days. On the other hand, it may be eminently chronic, and 
then the symptoms need not by any means be characteristic, 
and it may be the more difficult to make a diagnosis, as the in- 
crease in the size of the head is wont not to take place. Some- 



ABSENCE OF CERTAIN PARTS OF THE BRAIN. 309 

times the symptoms are those of brain tumor ; again those of a 
spastic spinal paralysis may predominate. 

The so-called hydrocephalus ex vacuo, a form which devel- 
ops in old people under the influence of a general atrophy of 
the brain, must also be looked upon as a secondary hydroceph- 
alus. It is associated with more or less pronounced demen- 
tia. About aetiology and treatment nothing need be added to 
what has been said on congenital hydrocephalus. 

Under certain circumstances there are found defects in the 
bony skull cap which allow the contents to protrude. By this 
the dura and galea as well as the skin are raised hemispheric- 
ally, constituting what is called a brain hernia or cephalocele, 
and we speak of an encephalocele if the brain substance and 
the pia are both contained in the dural sac, while, if only the 
dropsical soft meninges are to be found in it, it is called a men- 
ingocele. Whether a local decrease of resistance of the mem- 
branous skull and defects of ossification or perhaps abnormal 
adhesions of the meninges with the amnion is the cause of 
such anomalies has as yet to be decided. Clinically they pos- 
sess no significance. 

The above-mentioned defects (page 267), which we call por- 
encephaly (Heschl), may also be congenital. Some gyri may 
be entirely or partly absent, so that clefts or funnel-shaped 
openings or pits are formed. The defective areas, unless there 
be a communication with the ventricles, are covered with pia 
tissue, and the empty space is filled up with fluid which collects 
in the subarachnoidal tissue ; or, again, the neighboring convo- 
lutions are pressed together over the gap and instead of a hol- 
low we only find a deep cleft (cf. Ziegler, Pathol. Anat, ii, 636). 

Very remarkable is the fact that certain parts of the brain 
may be entirely absent. This has been observed for the corpus 
cailosum, the fornix, the corpora albicantia, the gray commis- 
sure, and others. With reference to the absence of the corpus 
cailosum various hypotheses have been put forward. It has 
been thought to be connected with the development of the 
base of the skull and to depend upon the angle which the 
petrous portions of the two temporal bones form with each 
other (Richter, Virchow's Archiv, 106, 1886). Recently Kauf- 
mann has described a case where the corpus cailosum was com- 
pletely absent and where its formation had never even begun, 
so that the commencement of the disturbance in development 



310 DISEASES OF THE BRAIN PROPER. 

had to be referred to a time between the third and fourth 
months. In this case the high grade of internal hydroceph- 
alus which was present had to be looked upon as the cause 
(Arch. f. Psych, und Nervenkrank., 1887, xix, Bd. iii, page 769). 
This, in all probability, is more frequently, than is generally 
supposed, the immediate cause of congenital malformations 
due to arrest of development which is principally the result of 
traumatism during birth, protracted labor, asphyxia in conse- 
quence of compression, etc. Deficiencies in the region of both 
fissures of Rolando are especially of interest because they may 
simulate in their clinical manifestations spastic spinal paralysis, 
although the resemblance is somewhat obscured by the simul- 
taneous presence of cerebral symptoms ; and there is, of course, 
every possible gradation, from the pure picture of a spastic 
spinal paralysis in which only the lower extremities are affected 
to that in which the arms are implicated and cerebral symp- 
toms are well marked. Schultze (Deutsche Medicinische 
Wochenschrift, 15, 1889) has observed the spastic rigidity in 
the lower extremities in more than one member of the same 
family. 

Sometimes certain parts of the brain are only imperfectly 
developed. Such a condition has been found in certain gyri, 
the optic thalami, the corpora quadrigemina, the corpora stri- 
ata, and others. Schroter, among other writers, has described 
such a defect in the corpus callosum, which in his case was 
abnormally short (Allgem. Zeitung f. Psych., 1888, xliv, 4, 5). 
The cerebellum may also remain very much behind in devel- 
opment, so that under certain circumstances it scarcely attains 
the size of a walnut. The causes of such local malformations 
are usually as obscure as their clinical manifestations during 
life. 



DISEASES OF THE SPINAL CORD. 



What we have said above about the diseases of the brain 
holds good, with certain limitations, also for those of the spinal 
cord. The anatomy of the cord certainly offers less difficulty 
than that of the brain, and, especially as regards the finer 
structure of the organ, has been more minutely examined into 
and is better understood ; but in the physiology there exist still 
so many points, some obscure, some still under discussion, that 
the pathology remains here also very incomplete. To give a 
description of the diseases of the spinal cord, especially when 
questions of its physiology and pathological anatomy are to be 
discussed, is an extremely difficult undertaking, and were it 
accomplished far better than I have been able to do it, would 
still stand in need of a lenient judgment. We shall adopt the 
same arrangement as in our account of the cerebral diseases, 
and divide the subject into three parts. The first will contain 
the diseases of the membranes of the spinal cord, the second 
those of the spinal or peripheral nerves, the third those of the 
white and gray matter of the cord. 



PART I. 

DISEASES OF THE SPINAL MENINGES. 

The spinal meninges are, on the whole, not frequently dis- 
eased alone ; more often the inflammation spreads from the 
(soft) membranes of the brain to the pia of the cord, or from 
the surrounding structures to the dura spinalis. The one of 
greatest practical interest among the affections of the meninges 
of the cord is the pachymeningitis cervicalis hypertrophica, 
which we Shall shortly describe. 

Of the anatomy but little needs to be added to what has been 
said on page 3. The spinal portion of the dura is thinner than 
the cerebral ; it widens into a large cylindrical sac, which is by no 
means filled up by the spinal cord. This dural sac extends beyond 
the lower end of the spinal cord (conus medullaris), and terminates 
in a cone-shaped point at the level of the second sacral vertebra ; 
all these are points too well known to be dwelt upon here at length. 
The conus medullaris ends in the filum terminate, a filiform process 
which is accompanied by the longitudinal nerve bundles coming 
from the lumbar and sacral portion of the cord, which constitute the 
cauda equina. The so-called ligamentum denticulatum is a flat band 
which by its inner edge is connected with the pia and externally by 
a toothed edge to the dura mater; the arachnoid lies in such close 
contact with the dura that the subdural space is only a capillary 
space, whereas the subarachnoid space, situated between the arach- 
noid and the pia, is of considerable width. The denticulate ligament 
divides it, though incompletely, into an anterior and a posterior 
half. In contradistinction to the pia mater of the brain, that of the 
spinal cord presents two different layers of connective tissue, the 
outer one of which, very well developed in man, passes into the sub- 
arachnoideal trabecule, while the inner is made up of a single layer 
of circular bundles of fibrillse (Schwalbe) {vide Fig. 96). 



INFLAMMATIONS OF THE DURA MATER. 



313 



CHAPTER I. 

INFLAMMATIONS OF THE DURA MATER. 

Pachymeningitis Spinalis. 

While in the cerebral portion of the dura the inner surface 
is the usual seat of the inflammation, we find that the spinal 
dura mater may be diseased on its outer as well as on its inner 
surface ; yet the clinical recognition and separation of these 
two forms is very often impossible. 

The inflammation of the outer surface of the dura, the 
pachymeningitis spinalis externa, or the inflammation of the 




Id. 



d. m. i. p. epd. s. sd. s. 

Fig. 96. — Cross-section through the Vertebral Column and the Spinal Cord 
(Diagrammatical), epd.s., epidural space, sd. s., subdural space, sar.s., subarach- 
noid space, i. p. , inner periosteum of vertebra, d. m. , dura mater, ad. , arachnoid, p. r. , 
posterior spinal root. /. d., denticulate ligament, a. r., anterior spinal root. (After 
Eichhorst.) 



connective tissue between the dura and the vertebral column, 
peripachymeningitis, is a very rare disease, and probably only 
occurs secondarily. The inflammatory changes, which at times 
are most marked on the posterior surface, consist of a thick- 
ening and cellular infiltration of the dura ; sometimes, also, 
the membrane may be found covered with dense cicatricial 
deposits (Eichhorst). The chief causes are caries or tuber- 
culosis of the vertebras, pleuritis, psoas abscess, syphilis, puer- 
peral pyaemia, suppuration in the peritoneal cavity, and in 
exceptional cases the disease may have its origin in a neuritis 



3i4 



DISEASES OF THE SPINAL MENINGES. 



migrans. The clinical picture depends largely upon the impli- 
cation of the nerve roots and of the spinal cord. If the cord is 
compressed by the thickening, the symptoms of a pressure pa- 
ralysis, to which we shall have occasion to refer later, make 
their appearance. If the nerve roots are implicated, there are 
violent paroxysmal pains which run along the vertebral column 
and radiate into the extremities. Rigidity of the neck and 
tenderness on pressure over the spinous processes of the verte- 
brae are rarely absent, but are not sufficient to warrant a diag- 
nosis, as they may be found just as well in an inflammation of 
the pia. To make a definite diagnosis will in all cases only be 
possible, if accompanying signs are taken into consideration, 
more especially those of any primary disease. It is always a 
difficult, sometimes even an impossible task. 

The inflammation of the internal surface of the dura mater 
usually develops in the cervical portion of the cord ; follow- 
ing Charcot, who first described the anatomical and clinical 



th.d. 



n.f. c. 




th.d. 



Fig. 97.— Cross-section through the Middle of the 'Cervical Enlargement in 
Pachymeningitis Cervicalis Hypertrophica. th.d., thickened dura, n.f.c, 
newly formed cavities, n. r., nerve-roots. (After Charcot.) 



features of the disease, it has been called pachymeningitis cer- 
vicalis hypertrophica ; the inflammatory new formation and 
thickening of the connective tissue, which are most marked on 
the posterior inner surface of the dura, exist in circumscribed 
areas (Fig. 97); this compresses the nerve roots, which pass 
through the membrane at these places, and finally even the 
cord, and may give rise to the formation of channel-like cavi- 



INFLAMMATIONS OF THE DURA MATER. 3^ 

ties {n.f. c. in Fig. 97). If the compression continues for a 
considerable time it leads to secondary degeneration of the 
pyramidal tracts in the spinal cord, as well as of the motor 
nerves originating in the parts diseased, and to atrophy of the 
muscles supplied by them. 

Symptoms. — The symptoms of the disease are mostly the 
outcome of the participation of the nerve roots and the spinal 
cord. The disease may well be divided into two stages, each 
having its characteristic symptoms. To the first belong the 
pains, to the second the paralyses (Charcot). The pains vary 
extremely in intensity and extent ; as a rule they are confined 
to the region of the neck, whence, occurring in paroxysms of 
increasing severity, they radiate into the upper extremities and 
are accompanied by paraesthesias in the arms, tingling and 
formication in the finger tips. The grip is usually markedly 
diminished, and a test with the dynamometer shows that the 
patient is able to lift only ten to fifteen kilogrammes. Not 
rarely trophic disturbances, in the form of vesicular eruptions, 
roughness and desquamation of the epidermis, are noted. The 
sensation of stiffness in the neck and of difficulty in moving the 
head troubles the patient a great deal, and gives to him a stiff, 
quite characteristic appearance. He carefully avoids turning 
his head in any direction, and tries to make up for this rigidity 
of his neck by turning the whole body, which he does slowly 
and in a somewhat awkward way. The most careful examina- 
tion of the cervical region, percussion of the spinous processes, 
hot sponges applied to the skin over them, and the like, does 
not always reveal an increased sensitiveness. 

Gradually, that is to say, in the course of two or three 
months or more, the patient gets accustomed to his pains, so 
much the more so as they become less severe in the further 
course of the disease. On the other hand, he discovers to his 
great distress that the motor power of his upper extremities is 
becoming more and more impaired. The stage of paralysis, as 
a rule, is immediately preceded by a peculiar heaviness and 
stiffness in the shoulder and elbow joints. The patients notice 
that they are unable to raise their arms as high as before ; if 
they are females, that they can not arrange their hair them- 
selves any more, owing to the impairment in the upward and 
backward motion of the arms, movements which finally become 
totally impossible. 

The elbow joint, too, becomes stiffened, and the motions 



316 



DISEASES OF THE SPINAL MENINGES. 



of the wrist and finger joints become visibly impaired. The 
disability is not, however, usually equal in both arms and 
hands, as one hand may be almost useless, while the function 
of the other is not much interfered with. Still, in some in- 
stances, the trouble may progress in both arms pari passu. 
Curiously enough, not all the muscles of the forearms become 
affected, but more especially those supplied by the ulnar and 
median nerves, w-hile the extensors, which are supplied by the 
musculo-spiral, remain more or less intact. The affection of 
the muscles manifests itself by an increasing atrophy and weak- 
ness, which allows an overaction of the healthy antagonists — 
the extensors — so that the hand, although by no means in all, 
but only in the well-marked cases, assumes a very character- 
istic position. It is dorsally flexed, and the fingers, which are 
bent in the second and third joints, give to it the appearance 
of a claw (Fig. 98). About the development of this position 




Fig. 98.— Position of the Hand in Pachymeningitis Cervicalis Hypertrophica. 
(Charcot.) 

we shall have more to say when speaking of the ulnar paraly- 
sis. The difficulties arising from this diminished motor power 
are considerably aggravated by the parassthesias in the finger 
tips. The patients are unable to take hold of small objects — 
pins, steel pens, etc. — they are unable to attend to their own 
toilet because they can not feel small buttons, and so forth. 
They become more and more helpless, and, what is of the 
greatest significance for patients belonging to the working 
classes, they become incapacitated for work and unable to earn 
their living. This may indeed be the case at quite an early 
period, when the patient is otherwise in a comparatively fair 



INFLAMMATIONS OF THE DURA MATER. 



317 



condition, especially in female patients who do fine hand-work 
(sewing, knitting, embroidering). The whole condition be- 
comes worse and worse. Arms and hands become stiffer and 
stiffer, until finally, although not in all instances, a complete 
paraplegia of the upper extremities develops. Whether or not 
to these symptoms a paresis or paralysis of the lower extremi- 
ties or bladder disturbances are added will depend entirely 
upon the extent to which the spinal cord takes part in the pro- 
cess. It can in no case either be predicted or excluded with 
certainty. 

Course. — The course of the disease is always chronic and 
extends over years. After the period of pains has passed the 
patients are, as a rule, free from them forever, and only suffer 
from the helplessness which results from the motor disturb- 
ances. Owing to this they require scrupulous care, have to 
be dressed, undressed, fed, etc., by an attendant. Recovery 
or even an improvement is an extremely rare outcome. To be 
sure, I have seen a cured patient in the clinic of Charcot, but 
from the minuteness with which this case was described, from 
the feeling of justifiable pride which accompanied the demon- 
stration, one could well see how extremely rare a cure must be. 
Remak, too, speaks of the curability of the disease (Deutsch. 
med. Wochenschr., 1887, No. 26). I myself am unable to pre- 
sent such a case. The patients in my wards, after unsuccess- 
ful trials of all proposed modes of treatment, have long given 
up all hopes of any marked improvement. 

Diagnosis. — The disease may, especially in its onset, possibly 
be confounded with either spinal leptomeningitis or, as we 
shall later show, with syringomyelia. It is natural that tumors 
of the vertebral column, if they be situated in the region of 
the cervical enlargement, should produce in the initial stage 
the same symptoms as a pachymeningitis. The further course, 
however, will soon settle the diagnosis. Besides these there 
are two more diseases which may in the mind of the beginner 
give rise to some difficulties with regard to the differential 
diagnosis — namely, progressive muscular atrophy and amyo- 
trophic lateral sclerosis. It is true that a patient with a pachy- 
meningitis may sometimes present the appearance of a man 
suffering from progressive muscular atrophy ; but the two dis- 
eases should never be confounded, inasmuch as in the latter 
affection the initial stage is not accompanied by pain, and the 
stiff neck has never been known to occur in it. The idea of 



3ii 



DISEASES OF THE SPINAL MENINGES. 



amyotrophic lateral sclerosis will probably also be discarded, 
as in this disease the lower extremities are implicated, and as 
difficulty in swallowing, a sign which indicates extension of the 
process to the medulla oblongata, will usually not be very late 
in appearing. We may say that the diagnosis of cervical 
pachymeningitis can, if the case is carefully examined and if 
the course of the affection is taken into consideration, almost 
always be correctly and definitely made out. 

./Etiology. — We are wholly ignorant of the aetiology of the 
disease. Some maintain that the abuse of alcohol is of some 
importance in this connection, others the living in damp houses. 
Whether syphilis has any such influence, and, if so, what is its 
mode of action, is not as yet established. There is no doubt that 
the affection is more common among the working classes and 
the lower grades of society, but what are the conditions and in- 
fluences which act as direct causes, if such there be, we are not 
able to say. 

Treatment. — The treatment comprises local as well as gen- 
eral therapeutic measures. The former consists of the applica- 
tion of strong counter-irritants — e. g., the painting twice daily 
with tincture of iodine, of the use of irritative ointments or 
moxas. The application of Paquelin's cautery, with which 
punctiform scars on the skin are produced (the so-called points 
de feu of the French), only deserves preference because it is 
less painful than the others. Any lasting result can not be ex- 
pected from it. Not more is effected by general or internal 
treatment, and it is impossible to give the indications for any 
particular remedy. Iodide of potassium has been used in order 
that something might be done, without, however, producing 
anything else than disorders of digestion. If the patient in- 
sists on taking medicine, a placebo ought to be given — acids, 
bitters, etc. In no case were we able to see any beneficial 
effects from warm baths and hydrotherapy in general. The 
only measure which at least modified the symptoms somewhat, 
in that it gave the patients for a time more freedom of motion 
in their paretic extremities, was electricity, more especially the 
cutaneous faradization with the brush on the neck as well as 
up and down the limbs. If the constant current is used it 
ought especially to be applied to the muscles innervated by the 
ulnar and median nerves. By repeated closing and opening 
of the current muscular contractions should be elicited. 



CHAPTER II. 

THE INFLAMMATIONS OF THE SOFT SPINAL MENINGES. 

Leptomeningitis Spinalis. 

The soft membranes are rarely ever by themselves the seat 
of inflammation, whether of an acute or a chronic type. Such, 
however, may exceptionally occur as the result of traumatism, 
of overexertion, carrying heavy loads, or as a consequence of 
exposure to cold after sleeping on the damp ground in camping 
out, etc. (Brown, cf. lit.). But in the greater number of cases 
we have to do with the extension of an inflammatory process 
of an infectious nature, as in epidemic cerebro-spinal menin- 
gitis, or in tubercular meningitis, both diseases which affect 
the membranes of the brain as well as those of the spinal cord. 
That there are instances of meningitis secondary to other dis- 
eases, and under what circumstances they occur, we have 
already stated on page 12. Here we only wish to draw at- 
tention to its connection with acute articular rheumatism, of 
which Krabbel (Inaugural Dissertation, Bonn, 1887) has re- 
ported an instance. 

Pathological Anatomy. — Pathologically the acute spinal 
meningitis is divided into three stages. The first is character- 
ized by a diffuse reddening and swelling of the meninges, more 
especially of the pia; the second by the appearance of a puru- 
lent or fibrino-purulent exudation upon this membrane. This 
may occur gradually, and may vary considerably in extent ; it 
may be found over the whole length of the pia (always more 
on the posterior surface), or may be confined to circumscribed 
areas. In the third stage the pus becomes reabsorbed and 
thickening of the pia with the formation of adhesions between 
it and the dura takes place. 

That the nerve roots also participate in the inflammation is 
evident from the hyperasmia of their blood-vessels, the infiltra- 
tion of the interstitial connective tissue, and the eventual de- 



320 



DISEASES OF THE SPINAL MENINGES. 



generation of the medullated nerve fibres. If we remember 
the many processes by which the pia is united with the spinal 
cord itself, it is not surprising that the latter is implicated. 
On cross-section it looks in places injected, cedematous, and 
is seen to bulge ; on the other hand, there are undoubtedly 
instances in which the cord does not take part in the inflam- 
mation. 

The chronic form, which seems very rarely to occur pri- 
marily, and then only after the protracted abuse of alcohol, is 
usually preceded by the acute disease or is secondary to differ- 
ent spinal lesions or various affections of the vertebrae. The 
pathological changes occurring here can well be compared 
with those of the acute form. In this condition we find thick- 
ening and opacity of the tissue, masses of newly formed con- 
nective tissue, and adhesions to the dura. There is turbidity 
of the spinal fluid, which is abnormally increased, and some- 
times abnormal formation of pigment. The brownish-red and 
black specks often seen are to be looked upon as the remains 
of previous haemorrhages, in which the coloring matter of the 
blood has undergone changes (Eichhorst). In consequence of 
the extraordinary development of the processes of the pia, this 
membrane adheres very firmly to the cord, so that it can not 
be stripped off without loss of substance of the cord. Here, 
again, the nerve roots are implicated, as is evident from their 
changed appearance. They look flattened and atrophic. 

Symptoms. — In the acute form pain undoubtedly plays the 
principal part. Even in the initial stage, which does not differ 
from that of other acute diseases in most of the symptoms 
(chill, general malaise, loss of appetite, disturbed sleep, ele- 
vation of temperature), the pain along the spinal column is 
very marked. The patients are constantly troubled with it in 
whatever position they may lie, although it is especially sharp 
on any attempt to move or to sit up in bed. At the same time 
they feel an unwonted stiffness in the muscles of the back, and 
have difficulty on motion. On careful examination of the back 
we find that, although the spinous processes of the vertebras 
are tender on pressure, and by the slightest tap or by the 
touch of a hot sponge pain is evoked, this is in no way com- 
parable to that felt by the patient without any extraneous in- 
terference. This persists obstinately, and usually in the further 
course of the disease may radiate into the arms and legs, 
owing, of course, to the implication of the nerve roots. The 



INFLAMMATIONS OF THE SOFT SPINAL MENINGES. 



321 



same factor also accounts for the different hyperaesthesias of 
the skin, the girdle sensation, the muscular pains, etc. Rigid- 
ity of the neck is only observed if the process has attacked the 
cervical portion. If the spinal cord itself becomes implicated, 
spinal symptoms, bladder disturbances, increased reflexes, and 
extensive sensory disturbances make their appearance. All 
these symptoms may persist unchanged for weeks, the patient 
feeling very bad, and complaining of constant violent pain. 
If the disease take a favorable turn the pains gradually abate 
and the patient gets relief ; but, on the other hand, the symp- 
toms of irritation may give place to those of paralysis, and as 
anatomical changes go on in the nerve roots (degeneration, 
atrophy), we have analgesias and anaesthesias, the muscles be- 
come more and more incapable of performing their functions, 
they undergo marked atrophy, and on electrical examination 
distinct reaction of degeneration is found. There is direct 
danger to life (1) if the process extends upward to the medulla 
oblongata ; in that case death may occur in a few days. (2) If, 
owing to an extensive myelitis, bed-sores develop which lead 
to the utter exhaustion of the patient. Recovery may be com- 
plete or incomplete ; in the latter case pareses, paresthesias, 
and bladder disturbances are left behind as the result of irrepa- 
rable anatomical changes. 

The symptoms of the chronic do not differ much from those 
of the acute form. The pains only are occasionally less pro- 
nounced. They vary with regard to their violence and seat ; 
sometimes they are most marked high up between the shoulder 
blades, sometimes lower down in the back, so as to interfere 
more or less completely with stooping ; not rarely they are 
found to radiate toward the front of the thorax, sometimes on 
one, sometimes on both sides. Even slighter degrees of pain 
are sufficient to seriously interfere with the occupation of the 
patient, especially, of course, if the arms or legs, or what is, 
however, rather rare, all four extremities are implicated. Sen- 
sory changes are found in both the acute and the chronic form ; 
an implication of the cord itself leads to the same symptoms 
of irritation or paralysis which we have before mentioned. 
The disease may drag out its course through a number of 
years and still there may follow a relative recovery ; complete 
recovery I have never seen. 

Diagnosis. — To make a correct diagnosis of this disease 
much experience and carefulness is necessary. Acute spinal 
21 



322 



DISEASES OF THE SPINAL MENINGES. 



meningitis may be mistaken for muscular rheumatism and 
lumbago, the chronic form for spinal irritation and cord dis- 
eases. A differentiation from the former may be facilitated by 
an examination of the spinous processes for tenderness on tap- 
ping or touching with a hot sponge. In simple muscular 
rheumatism the spinous processes are not sensitive, whereas 
the different muscles are found to be tender if pressed or 
kneaded. Lumbago pains are recognized by their greater 
severity, their frequent change in locality, and their lesser 
persistency. Spinal irritation should only be diagnosticated 
in very anaemic hysterical individuals; and the further course 
and final outcome of the disease will guard us against the as- 
sumption of the existence of a cord disease, for, if this be 
present, the issue is always unfavorable. 

Treatment. — With reference to treatment little is to be 
added to what has been said on page 318. Here, too, local 
measures — counter-irritation, etc. — must first be tried, and in 
case they should be found of no avail, prolonged tepid baths 
(93 Fahr., for from half an hour to an hour and a half) should 
be substituted. Electricity should also be used in the form of 
the faradic brush applied over the painful muscles. Gentle 
massage, if practiced by a competent person, is strongly to be 
recommended, and ought to be continued for a long time. 
The administration of iodide of potassium, for which no indi- 
cation whatever exists, is to be condemned. 



CHAPTER III. 

HEMORRHAGE INTO THE SPINAL MEMBRANES MENINGEAL APOPLEXY 

PACHYMENINGITIS INTERNA HEMORRHAGICA. 

The vessels nourishing the spinal meninges are the anterior and 
posterior spinal arteries, arising from the vertebral artery, which in 
its turn comes off from the subclavian. They join with a succession 
of small branches which enter the spinal canal through the interver- 
tebral foramina and form median vessels, which run in front and 
behind the cord along the longitudinal fissure, having numerous hori- 
zontal anastomoses. Both of these arteries send constantly fine 
horizontal twigs into the substance of the cord, while others are dis- 
tributed to the pia. The capillary network is decidedly denser in 
the gray than in the white matter. 

The occurrence of a haemorrhage between the membranes 
of the spinal cord (" intrameningeal "), or between the dura 
and the bony vertebral canal (" extrameningeal "), is, on the 
whole, very rare. If one of these two forms occurs more fre- 
quently than the other, it is the latter, the extrameningeal, the 
so-called apoplexia epiduralis, so named because the blood es- 
capes into the epidural space (cf. Fig. 96). The haemorrhages 
between the dura and the arachnoid— apoplexia subduralis — 
and those between the arachnoid and the pia — apoplexia sub- 
arachnoidal — which break into the space filled with the 
cerebro-spinal fluid, are much more uncommon. If we find on 
the inside of the dura encapsulated foci of variable size which 
contain products of decomposition, haematoidin crystals, de- 
tritus, etc., then we speak of a pachymeningitis interna hasmor- 
rhagica. The loose blood coagula may be found of such a size 
that they compress the cord and the nerve roots. On the 
other hand, there may be nothing more than punctiform ex- 
travasations of blood, in the neighborhood of which the vessels 
of the dura appear more than usually full. That these coagula 
are to a certain extent capable of being absorbed, and that 



324 DISEASES OF THE SPINAL MENINGES. 

they do not necessarily irreparably damage the cord and the 
nerve roots, is proved by the cases which take a favorable 
course. 

etiology. — With reference to the aetiology, it may be said 
that such haemorrhages may be evoked by overexertion. They 
occur by preference in men, and more especially in laborers 
who do hard work, such as carrying heavy loads, and who 
drink a great deal of alcohol. Further, after traumatic influ- 
ences, either direct injury to the bodies of the vertebrae or 
after severe concussions affecting the whole body, such as one 
might receive, for instance, in a collision between two railroad 
trains, in which case symptoms arise which simulate very 
much the clinical appearances of railway spine, which we shall 
describe later. Secondary meningeal apoplexies occur in the 
course of infectious diseases — scarlet fever, small-pox, typhoid 
fever, etc. Also in epileptics they are not rare, and, according 
to Hasse, are often associated with heart hypertrophy. 

Symptoms. — The symptoms very closely resemble those of 
spinal meningitis, only that the onset is always very sudden — 
"apoplectiform." A person in perfect health may feel sud- 
denly a violent circumscribed pain in the back which differs in 
degree and extent in different cases, and which if the haemor- 
rhage is extensive may in a few hours give place to complete 
paralysis of the legs (more rarely of the arms). In milder 
cases, while the pains gradually abate, sensory disturbances, 
paraesthesias and anaesthesias, gradually develop, also slight 
motor disorders, weakness in the muscles of the extremities, 
sometimes also signs of motor irritation — trembling, twitching, 
etc.' The main characteristic of a meningeal haemorrhage 
which is purely spinal is the complete freedom from disturb- 
ances of consciousness. The course and the duration of the 
disease depend upon the extent of the haemorrhage and its 
capability of being absorbed. It is necessary to have seen, 
carefully studied, and analyzed several cases of this nature in 
order to properly understand and correctly recognize a new 
instance. The implication of the spinal cord itself necessarily 
gives rise to what are known as " spinal symptoms " (increased 
reflexes, bladder disturbances, persistent paralyses), as we have 
repeatedly stated. 

Diagnosis. — The diagnosis is easy in the cases with charac- 
teristic onset if we are satisfied with the diagnosis of " menin- 
geal apoplexy," whereas it is very difficult, nay, often impossi- 



MENINGEAL APOPLEXY. 



325 



ble, to determine the exact kind, whether it is epidural or sub- 
dural. Again, to determine its situation is comparatively easy 
if we remember that in affections of the lumbar cord the legs, 
bladder, and the rectum mainly suffer, whereas affections of 
the dorsal region give rise to symptoms of irritation in the dis- 
tribution of the intercostal nerves, and those of the cervical 
portion to motor and sensory disturbances in the upper ex- 
tremities. If the seat be still higher up — in the medulla ob- 
longata — bulbar symptoms, disorders of respiration and deglu- 
tition, will not be absent, and the case will be fatal in a short 
time. 

Prognosis. — The prognosis depends upon the extent of the 
hsemorrhage. Cases with a favorable outcome have repeatedly 
been observed. Implication of the cord and the nerve roots 
makes the prognosis more unfavorable. 

Treatment. — In the treatment we ought in a fresh case, in 
the first place, to procure absolute rest in bed and apply ice 
over the supposed seat of the trouble, to arrest the haemorrhage 
if possible or to prevent the return of it. If the irritation seems 
to be localized, local bleeding may be indicated. The further 
treatment is the same as in acute meningitis. 

Tumors of the spinal meninges are of no practical impor- 
tance, because they can never be diagnosticated with certainty. 
Although we know well from the reports of autopsies that just 
as in the cerebral we may in the spinal meninges find psammo- 
mata, sarcomata, myxomata, gummata, carcinomata, etc., and 
that their seat may be epidural, subdural, and subarachnoidal, 
we are never able to recognize definitely from the symptoms 
observed during life either the nature or the seat of a tumor in 
the meninges of the cord. The reason is very simple. The 
tumors, as long as they are very small, produce no symptoms, 
and if they grow give rise to symptoms which depend upon 
the compression of the cord and the nerve roots and can not 
be distinguished from those produced by pachymeningitis and 
leptomeningitis spinalis. They consist therefore of signs of 
motor and sensory irritation and later of paralysis, which vary 
according to the seat of the tumor. If, for instance, only one 
half of the cord is compressed, this may give rise to a clinical 
picture which resembles that of a unilateral lesion of the spinal 
cord — viz., paralysis and hyperesthesia on the side of the com- 
pression, anaesthesia on the intact side. A case of this kind 



326 



DISEASES OE THE SPINAL MENINGES. 



has been reported by Charcot (cf. lit.). Innumerable variations 
are possible, according to the size and seat of the tumor, and 
the less we are able to fully diagnosticate the cases during life 
the more important and instructive it will be to examine and 
describe as carefully as possible what is found at the autopsy. 

LITERATURE. 

Braun. Bemerkungen liber die Meningitis spinalis, besonders nach Feldziigen, 

bei Officieren. Deutsche militararztl. Zeitschr., 1872, i, 3, 4, p. 116. 
Leyden. Klinik der Riickenmarkskrankheiten. Berlin, 1874, 1, pp. 443 et seq. 
Charcot. Klinische Vortrage iiber Krankheiten des Nervensystems. Deutsch 

von Fetzer. Stuttgart, 1878, ii, 83 et seq. 
Braubach. Archiv f. Psych, und Nervenkrankheiten, 1884, xv, 3, 489. (Lipoma 

of the spinal meninges.) 
Hirtz. De la pachymeningite cervicale hypertrophique curable. Arch, gener., 

June, 1886, p. 641. 
Raymond. Des differentes formes de lepto-my6htes tuberculeuses. Revue de 

m6d., March, 1886, vi, 3. 
Senator. Ueber einige Falle von epidemischer Cerebrospinalmeningitis, etc. 

Charite-Annalen, 1886, xi, p. 288. 
Henoch. Zur Pathologie der Cerebrospinalmeningitis. Ibid., 1886, p. 525. 
Weichselbaum. Fortschritte der Med., 1887, v, 19. 
Eichhorst. Handbuch der speciellen Pathologie und Therapie, 3. Auflage. 

Wien und Leipzig, 1887, iii, 266 et seq. 
Goldschmidt. Centralbl. f. Bacteriologie und Parasitenkunde, 1887, ii, 22, p. 

649. (On diplococcus intracellularis meningitidis.) 
Maguire. A Case of Idiopathic Suppuration of the Spinal Dura Mater. Lancet, 

July 7, 1887, p. 9. 
Cramer. Ueber multiple Angiosarcome der Pia mater spinalis mit hyaliner De- 
generation. Inaug. Diss. Marburg, 1889. 



PART II. 

DISEASES OF THE SPINAL NERVES. 

The nerves of the spinal cord, which are called spinal or periph- 
eral nerves, arise, as is well known, by an anterior smaller, and a 
posterior larger root. These are flat bundles of fibres, loosely sur- 
rounded by the arachnoid, which pass into the intervertebral foram- 
ina, where the posterior roots form a swelling, the ganglion inter- 
vertebrale, and emerge from the spinal canal, the two roots having 
united to form a common round trunk. This again divides after its 
exit from the canal into two branches, an anterior and a posterior. 
The anterior, usually the larger, forms numerous anastomoses with 
the branches above and below it, the so-called ansae, which are col- 
lectively called plexuses. The posterior, smaller nerves, pass back- 
ward between the transverse processes of the vertebras, and are 
distributed to the muscles and the skin of the back. 

Of the thirty-one pairs of spinal nerves, there are eight cervical, 
twelve dorsal, five lumbar, five sacral, and one coccygeal. The pos- 
terior as well as the anterior branches contain fibres from both roots. 
The anterior roots are motor (Charles Bell, 1811). They supply, 
besides all the muscles of the trunk and extremities, the unstriped 
muscles of the internal organs and the unstriped muscles of the 
vessels. The posterior roots are sensory, but we should keep in 
mind that the anterior most probably contain, besides the motor, 
also trophic and secretory, and the posterior roots, besides the sen- 
sory, also fibres for the reflexes. 

The peripheral nerves, just as the cranial, may be affected 
independently or secondarily, and as the result of some primary 
disease in other parts. In cases of the first class overstrain 
plays an important role, often also, as we have seen to be the 
case in diseases of the cranial nerves, exposure to cold and 
traumatism, while in those of the second class a great many 
factors come in, more especially infections, intoxications, and 
general cachexias ; of these we shall speak when we treat of 
the individual nerves. 



228 DISEASES OE THE SPINAL NERVES. 

If we inquire into the anatomical character of the disease 
we shall in many instances have to admit that we are unable 
to find any anatomical changes whatever in the affected nerves. 
This is true in many cases of mild neuralgias, but also in some 
of the severe, even of the severest, types. The examination of 
pieces of the trigeminus, for instance, which were cut out 
where a resection had been made on account of intolerable 
pain has by no means always revealed appreciable changes in 
the nerve ; on the contrary, this has on microscopical, as well 
as on macroscopical, examination repeatedly been found to be 
absolutely normal. In other instances, however, an inflamma- 
tion — i. e., a neuritis — could be demonstrated as having been 
the cause of the trouble. In such cases there is seen in the 
acute stage an exudation in the interstitial tissue and an abun- 
dant infiltration of the same with round cells, a condition which 
gives rise to a swollen and cedematous appearance of the nerve 
(" purulent neuritis "). If this inflammation continues for some 
time the process goes on to degeneration, under the influence 
of which a part of the myeline sheath is destroyed and com- 
pound granular corpuscles are formed. The axis cylinders 
generally remain for some time intact. In some bundles there 
may be found nerve fibres completely atrophied, while the 
sheath is somewhat thickened and irregularly contracted, pre- 
senting a wavy outline. This increase and condensation of 
the connective tissue makes the nerve look more and more 
like a cord of connective tissue, which is thinner or thicker 
than normal according to the amount of the newly formed 
tissue ; sometimes, also, it is in places irregularly thickened 
(neuritis nodosa). The pigment deposits found have to be 
looked upon as the remains of previous hemorrhages. Even 
after extensive destruction of the nerve fibres by the connect- 
ive tissue, regeneration is to a certain degree possible, as the 
peripheral nerves possess this power to a considerable extent, 
a point which is of importance for the prognosis. According 
as the advance of the process is centrifugal or centripetal we 
speak of a descending or an ascending neuritis. A neuritis 
migrans has also been described. If the process occur simul- 
taneously at different places, we speak of a multiple or a dis- 
seminated neuritis (Leyden, Roth). From the researches of 
Scheube we should be led to regard the so-called beri-beri, or 
kak-ke, a disease which occurs epidemically in Japan, as a 
multiple neuritis. In very chronic cases the inflammatory 



DISEASES OF THE CERVICAL NERVES. 



329 



changes in the connective tissue are so slight in comparison to 
the degenerative process in the nerve fibres that it is prefera- 
ble to speak in those cases (as Striimpell has proposed) of a 
" primary chronic degenerative atrophy of the nerves," instead 
of a neuritis. 

The symptoms of neuritis, of course, vary according to the 
position and the function of the affected nerve, as we shall 
show in the following pages. The symptomatology of the 
primary multiple neuritis par excellence we shall describe later. 

The peripheral nerves may also be the seat of neoplasms, 
which in them usually develop, starting from the connective 
tissue. Only rarely do they consist of newly formed nerve 
fibres, and deserve properly to be called neuromata ; much 
more frequently they are fibromata, which may be found as 
solitary or as multiple new growths, and which not uncom- 
monly may give rise to thickenings and nodular swellings, 
which can be easily demonstrated and felt on the nerves. Ex- 
tensive tumors, where numerous nerve trunks are united by 
connective tissue into a compact mass, the so-called plexiform 
neuro-fibromata, are rare. Malignant neoplasms, carcinomata, 
and sarcomata of the peripheral nerves are sometimes met 
with. That here, also, the symptoms depend on the seat of 
the new growth is self-evident (cf. Krause on Malignant Neuro- 
mata and the Occurrence of Nerve Fibres in them. Volk- 
mann'sche Sammlung klin. Vortrage, 293, 294, 1887. Deutsche 
med. Zeitung, 1888, No. 15). 

We shall first speak of the affections of the motor and the 
sensory nerves which -innervate the muscles of the extremities 
and the trunk, and certain internal organs which are not con- 
nected with the cranial nerves, and after that we shall turn our 
attention to the trophic, the vaso-motor, and the secretory 
fibres as far as our scanty knowledge on these points will 
allow. An appendix will be devoted to the primary affections 
of the muscles supplied by the spinal nerves. 

A. Diseases of the Motor and Sensory Nerves. 

/. Diseases of the Cervical Nerves. 

Of the four upper (smaller) cervical nerves, the first, which is 

called the suboccipital, emerges between the occipital bone and the 

atlas. The anterior branches of these four form the plexus known 

as the plexus cervicalis, which is situated opposite the correspond- 



33Q 



DISEASES OF THE SPINAL NERVES. 



ing vertebrae. From this plexus come, besides the muscular branches 
to the scalenus, the longus colli, etc., the phrenic, which chiefly is 
formed by the fourth cervical nerve, and which for the most part 




Fig. 99.— Diagrammatic Outline of the Cervical and Brachial Plexuses. (After 
Schwalbe.) CI -VI II, roots of the cervical nerves. DI-III, roots of the first three 
dorsal nerves, pp, posterior branches— / 2 , of the second, p 3 , of the third cervical 
nerve. 1, anterior branch of the first cervical nerve and loop of union with the second. 
2, small occipital nerve. 3, great auricular nerve. 3,, superficial cervical nerve. 3«, 
communicating branches to the descendens noni from the second and third. 36", com- 
municating to the accessorius from the third and fourth nerves. 4, supraclavicular nerves. 
4 /t phrenic nerve. Brachial plexus: V l -VIII i , and D ; , the five roots of the brachial 
plexus. 5, rhomboid nerve. 5, suprascapular. 5^, posterior thoracic. 6, nerve to the 
subclavius muscle. 7, 7,, inner and outer anterior thoracic nerves. 8, 8,, 8,,, subscapu- 
lar nerves. MC, musculo-cutaneous. M, median. U, ulnar. MS, musculo-spiral. ic, 
internal cutaneous. JV, nerve of Wrisberg. c, circumflex, z, i, intercostal nerves. ih, 
intercosto-humeral nerve. 



is a motor nerve, the superficial cervical, the auricularis magnus, the 1 
occipitalis minor, and several communicating branches to the upper 
cervical ganglion and the gangliform plexus of the vagus (Figs. 99 
and 100). 



THE CERVICAL PLEXUS. 



331 



The anterior branches of the four lower (the stouter) cervical 
nerves, after they have passed between the anterior and middle 




Fig. 100. — The Superficial Branches of the Cervical Plexus. (After Hirsch- 
feld and Leveille.) i, superficial cervical nerve; 2, its inferior branch; 3, its supe- 
rior branch ; 4, its union with the facial. 5, great auricular nerve ; 6, one of its facial 
branches ; 7, its branch to the lobule ; 8, twig which pierces the auricle to pass to its 
outer surface ; 9, branch to the deep surface of the pinna ; 10, its union with the poste- 
rior auricular of the facial nerve. 11, small occipital nerve ; 12, its branch which unites 
with the great occipital nerve ; 13, a mastoid branch or second small occipital ; 14, twigs 
from this to back of the neck. 15, inner, 16, 17, middle, 18, outer branches of the supra- 
clavicular nerves. 19, branch of cervical nerves passing into trapezius muscle. 20, ac- 
cessorius spinalis. 21, branch to the levator scapula?. 22, trunk of the facial nerve ; 2j, 
its posterior auricular branch ; 24, its inframaxillary branch. 25, great occipital nerve. 

scalenus and have reached the supraclavicular fossa, form, in con- 
junction with the anterior branch of the first dorsal nerve, the so- 



332 



DISEASES OF THE SPINAL NERVES. 



called brachial or subclavian plexus (Fig. 101), which may be divided 
into a smaller or supraclavicular portion, situated above, and a larger 
infraclavicular portion situated below the clavicle. From the former 
are given off, besides the suprascapular, only the three subscapular 




Fig. ioi. — Deep Dissection of the Axilla, showing the Brachial Plexus. (After 
Hirschfeld and Leveille.) i, vagus. 2, phrenic, passing down to the inner side of 
the scalenus anticus muscle. 3, posterior thoracic nerve distributed to the serratus mag- 
nus. 4, external anterior thoracic nerve passing into the pectoralis major. 5, supra- 
scapular nerve. 6, musculo-spiral nerve. 7, ulnar nerve. 8, median nerve. 9, muscu- 
locutaneous nerve. 10, small internal cutaneous nerve (nerve of Wrisberg). 



nerves, the anterior and posterior thoracics, and the rhomboid nerve. 
The larger portion, which has also been called the axillary plexus, 
furnishes the large nerves which supply the entire upper extremity, 
the circumflex (axillaris), the median, the ulnar, the musculo-spiral 
(radial) and cutaneous branches, namely, the nerve of Wrisberg, the 



THE BRACHIAL PLEXUS. 



333 



internal, and Che (longest) external or musculo-cutaneous nerve, 
which has also been called perforans Casseri (cf. Figs. 102 and 103). 





Fig. 102. Fig. 103. 

Fig. 102.— Cutaneous Nerves of the Shoulder and of the Upper Arm. (After 
Hirschfeld and Leveille.) 1, 1, supraclavicular nerves from cervical plexus. 2, 2, 
2, cutaneous branches of the circumflex nerve. 3, 4, upper branches of internal cutane- 
ous nerve. 5, upper external cutaneous branch of musculo-spiral. 6, internal cutane- 
ous nerve. 7-10, branches of the internal cutaneous nerve. 11, musculo-cutaneous 
nerve. 12, lower external cutaneous branch of musculo-spiral nerve. 

Fig. 103.— Cutaneous Nerves of the Forearm and of the Palm of the Hand. 
(After Hirschfeld and Leveille.) 9-11, as in Fig. 102. 12, cutaneous branches of 
the musculo-spiral nerve. 13-14, further branches of the internal cutaneous nerve. 15 
and 16, terminal branches of the musculo-cutaneous nerve. 17, the radial nerve. 18, 
palmar cutaneous branch of median nerve. 19-23, digital branches of the median nerve. 
24 and 25, digital branches of the ulnar nerve. 



Just as we have seen in speaking of the cranial motor 
nerves — e. g., the oculo-motorius, the abducens, and the facial 
— the motor disturbances of the spinal nerves may be of a 



334 DISEASES OF THE SPINAL NERVES. 

paralytic or of an irritative character. In the former case the 
mobility of the muscles supplied by the affected nerve is di- 
minished (paresis) or completely lost (paralysis). In the latter 
we have symptoms of motor irritation which are not under the 
control of the will, the so-called spasms. These consist either 
of transient muscular contractions or of a lasting state of spas- 
modic contraction of one or of several muscles. The former 
we call clonic, the latter tonic spasm. 

On the whole, paralytic symptoms are much more common 
in the distribution of these plexuses than symptoms of irri- 
tation. 

In the sensory disturbances we can equally distinguish 
paralytic from irritative conditions, the former giving rise to 
anaesthesia, the latter to hyperesthesia. The anaesthesia is 
characterized by the fact that external (mechanical, chemical, 
or thermic) stimuli are either not perceived at all or with di- 
minished acuteness, whereas in hyperesthesia, on the contrary, 
even very weak stimuli are felt to be abnormally strong and 
unpleasant. The latter condition is usually attended with 
symptoms of sensory irritation, namely, either by pronounced 
pains or by paresthesias — that is, abnormal sensations of prick- 
ing, formication, numbness, or a " furry feeling." 

The affections of the sensory fibres of the spinal nerves 
chiefly manifest themselves by symptoms of irritation. They 
are always associated with more or less pain and are called 
neuralgias. That these also occur in the cranial nerves has 
already been stated, and the trigeminal neuralgia (cf. page 68) 
may be taken as a type of them. The neuralgic pains are 
usually very violent, but are rarely or never constant. They 
appear periodically and follow fairly accurately the distribu- 
tion of the affected nerve. The diagnosis is rarely difficult. 
Peripheral anesthesias — that is, such as are only due to affec- 
tions of the peripheral nerves or their end organs — are, as we 
said, rare. 



CHAPTER I. 

LESIONS OF THE CERVICAL PLEXUS. 

The cervical plexus is, on the whole, much less frequently 
affected with motor disturbances than the brachial Among 
the nerves belonging- to it, it is especially the phrenic which 
may present symptoms of paralysis or of irritation ; yet neither 
paralysis nor spasm of the diaphragm due to disease of the 
phrenic is of any great practical importance, since neither 
affection scarcely ever occurs by itself, but is much more often 
met with only when associated with other diseases. Paralysis, 
for instance, is observed in the course of progressive muscular 
atrophy, in hysteria, probably also in lead poisoning. Trauma- 
tism or mechanical compression produced by tumors or ab- 
scesses in the neck ma)' be the cause. Among the signs of 
paralysis of the diaphragm there is chiefly one which is very 
conspicuous — namely, the faulty expansion in the epigastric 
region during inspiration. Instead of becoming prominent, as 
is the case in the normal condition, the epigastrium is drawn 
in, and when we lay our hand on it we can feel that the dia- 
phragm does not descend. If only one of the phrenic nerves 
is thus affected this phenomenon is present only on one side, 
while the other half of the diaphragm performs its function 
properly. Besides this, hardly any other symptoms are ob- 
served in uncomplicated cases if the patient remains at rest, 
whereas if he exerts himself a distinct dyspnoea and an increase 
in the frequency of the respiration become apparent. The ob- 
stinate constipation which such patients complain of can well 
be understood if we remember the part which the diaphragm 
takes in the abdominal pressure. 

Spasm of the diaphragm, at least the tonic form of it, is not 
more common than paralysis. Patients affected with this suffer 
from great shortness of breath and quickly become cyanosed. 
The markedly prominent epigastrium remains with the dia- 



336 



DISEASES OF THE SPINAL NERVES. 



phragm immobile and is tender to the touch, and only the upper 
part of the thorax shows shallow respiratory movements. In 
some cases of tetanus, tonic spasm of the diaphragm seems to 
be the cause of death. It occurs almost never by itself with- 
out some accompanying or underlying affection, except in hys- 
terical persons. On the other hand, the clonic form of the 
spasm, the so-called hiccough (singultus), is extremely common. 
Everybody is familiar with the short clonic movements of the 
diaphragm, which are accompanied by inspiratory sounds and 
which vary in frequency and severity, occurring sometimes in 
such rapid succession that eighty or even a hundred may be 
counted in one minute. Severe protracted hiccough may be- 
come very troublesome, indeed, even dangerous, if sleep is for 
a long time seriously interfered with. This is, however, only 
the case if singultus occurs as a symptom in the course of 
other diseases — e. g., in apoplexy, in peritonitis, in chronic gas- 
tric catarrh, etc. As a rule it is arrested without any interfer- 
ence on the part of the physician by popular methods, such as 
holding the breath, closing the glottis, and then attempting an 
expiration. 

Therapeutics is almost powerless in the face of affections 
of the motor fibres of the phrenic. In paralysis electrical stim- 
ulation of the nerve, in the (tonic) spasm chloroform and mor- 
phine have been recommended ; yet these measures have by 
no means been effectual. 

The sensory fibres which the phrenic takes up in its course, 
and which are distributed to the pleura, the pericardium, and 
the peritonaeum, may also be affected. Neuralgia of the 
phrenic is rare, or perhaps we had better say is undoubtedly 
but rarely recognized. The pains, starting at the base of the 
thorax at the points corresponding to the insertions of the 
diaphragm and radiating in all directions, are taken for rheu- 
matism of the chest muscles or intercostal neuralgia, and it is 
only in cases where the pain is felt directly over the scalenus 
anticus and corresponds to the course of the nerve that the 
diagnosis is made correctly. Valleix's painful points can occa- 
sionally be demonstrated on the spinous processes of the 
upper cervical vertebras and at the points of insertion of the 
diaphragm. Respiration is only interfered with if the mobility 
of the diaphragm is at the same time impaired. 

The aetiology of the disease is obscure ; more especially are 
we ignorant of the conditions under which it may occur in- 



LESIONS OF THE CERVICAL PLEXUS. 



337 



dependently. It seems not to be a rare accompaniment of 
Graves' disease, of angina pectoris, and of sclerosis of the 
coronary arteries. 

Another apparently more important neuralgia in the region 
of the cervical plexus is the occipital or cervico-occipital neu- 
ralgia, which attacks by preference the occipitalis major, but 
also the minor, further the auricularis magnus (cf. Fig. ioo), 
and the superficial cervical. The patients complain of pain in 
the whole occipital region, in the neck, often, too, in the ears. 
Much more rarely the pain radiates in a forward direction to 
the cheek and the lower jaw. In the intervals the sufferer is 
perfectly comfortable, while during the attacks the pain be- 
comes very intense, although it never reaches the pitch of 
some trigeminal neuralgias. Such patients dread every motion 
of the head and carefully avoid every cause for laughing, as 
this, as well as sneezing, chewing, and so forth, is liable to 
bring on an attack. The consequent rigid position of the neck 
is quite characteristic for this form of neuralgia. Painful points 
can sometimes be found at the exit of the occipitalis major — 
that is, about halfway between the mastoid process and the 
spinous processes of the cervical vertebra?. Where they are 
absent the disease may be confounded with torticollis rheu- 
matica ; yet such a mistake may be avoided by remembering 
that the neuralgia is not constant, but characterized by in- 
tervals of perfect ease. 

The course of an occipital neuralgia is often tedious, but, 
on the whole, it is not unfavorable, and complete cures are not 
rare. The prognosis is only bad if there be some organic lesion 
of the nerve, caused, for instance, by disease of the cervical 
vertebrae. If, too, as is usually the case, no definite cause can 
be found, energetic counter-irritation to the skin, local bleed- 
ing, or galvanization, are sufficient to effect a cure or at least 
an improvement. Subcutaneous injections of morphine we 
shall probably in most cases be able to dispense with. The 
removal of every deleterious cause should, of course, be in- 
sisted upon. Under certain circumstances the occupation has 
something to do with it. Thus, I have found that the steve- 
dores of the London docks, who carry extremely heavy weights 
on their backs which press upon the neck and the occiput, are 
frequently subject to occipital neuralgia (cf. Hirt, Krankheiten 
der Arbeiter, iv, 91). 



CHAPTER II. 

LESIONS OF THE BRACHIAL PLEXUS. 

The brachial plexus may be diseased in its supra- or infra- 
clavicular portion. The affections of the latter, undoubtedly 
the more frequent, are of greater practical importance than 
those of the former. 

Here, too, the motor disturbances are more prevalent, sen- 
sory disturbances in the region of the brachial plexus, espe- 
cially neuralgias, being decidedly exceptional. 

In the supraclavicular portion, above all, the posterior tho- 
racic — which, coming from the fifth and sixth cervical nerves, 
supplies the serratus magnus — is affected in an interesting and 
very striking manner. 

The so-called serratus paralysis is quite frequently due to 
the calling of the patient, as certain occupations seem particu- 
larly to predispose to it. If prolonged pressure is frequently 
exerted on the nerve — as, for instance, is the case in people 
who carry heavy loads on their shoulders, or if the shoulder 
muscles, especially the serratus, are overexerted, as happens, 
for instance, in mowing, in certain manipulations of tailors, 
shoemakers, etc. — the paralysis has been known to develop 
rapidly. Occasionally such ^etiological factors are absent and 
we are forced to fall back upon the still obscure influence of 
what is called "catching cold." 

The condition is quite characteristic whether the arm be in 
a state of motion or at rest. In the latter position the scapula 
appears elevated and approaches with its lower angle the ver- 
tebral column more than normally, the inner median margin 
having an oblique upward and outward direction. The cause 
of this deformity is to be sought in the overaction of the an- 
tagonists — the rhomboids, the levator anguli scapulas, and the 
trapezius (Fig. 104). On moving the arm, the patient, we find, 
can raise it only to the horizontal position, owing to the absence 



LESIONS OF THE BRACHIAL PLEXUS. 



339 



of the action of the serratus, which pushes the scapula forward. 
As soon as we produce artificially the action of this muscle by 
fixing the shoulder blade and pushing it forward, complete 
elevation of the arm is possible. If the patient attempts this 
same motion himself the scapula is approached to the spinal 




Fig-. 104. — Case of Right-sided Serratus Paralysis in a Man Thirty-five Years 
of Age. Position of the scapula with the arm hanging down. (After Eichhorst.) 



column. If the arm is raised in front of the chest the inner 
edge of the scapula is elevated and stands off from the thorax 
in a wing-like fashion, so that we are able to touch the inner 
surface of the bone (Fig. 105). This appearance, which is very 
characteristic, is perfectly sufficient in conjunction with the 
other signs to assure the diagnosis. Besides a moderate im- 
pairment in adduction, which somewhat interferes with the fold- 
ing of the arms across the chest, there are no other abnormi- 



340 DISEASES OF THE SPINAL NERVES. 

ties to be mentioned. Especially is it to be noted that there 
are no decided sensory changes to be perceived in a pure ser- 
ratus paralysis. As this affection is not rarely met with in the 
course of progressive muscular atrophy — sometimes this dis- 
ease begins with a serratus paralysis — it is not to be wondered 




Fig. 105. — The same Case with the Arms raised. 

at that the muscle at fault is sometimes found to be wasted. In 
the traumatic paralysis the atrophy comes on very late — many 
years after the traumatism. The muscle remains intact, elec- 
trical reactions are normal — reaction of degeneration being by 
no means always demonstrable — and yet there is no improve- 
ment. The prognosis, on the whole, is bad ; the disease even 
in the most favorable cases is of very long duration, and may 
last for weeks, months, or years. Often it is not curable at 



LESIONS OF THE BRACHIAL PLEXUS. 



341 



all, and the patient is, as it were, maimed for the rest of his 
days. 

Not too much hope ought to be placed in the electrical 
treatment, no matter in what form electricity be employed; in 
grave cases, at least, such hopes are doomed to disappoint- 
ment. 

The paralyses of the pectoralis major and minor (anterior 
thoracic nerves), of the rhomboidei and the levator anguli 
scapulas (muscular branches from the third, fourth, and fifth 
cervical nerves), of the latissimus dorsi, subscapulars, and 




Fig. ic6.— Position of the Head in Spasm of the Splenius Capitis on the Right 

Side. 



teres major (subscapular nerves), finally, those of the supra- 
spinatus and infraspinatus (suprascapular nerve) have alone no 
practical importance, and will as far as is necessary be men- 
tioned in the consideration of progressive muscular atrophy. 
A lesion of the left suprascapular has been described by Hoff- 
mann, one of the right by Bernhardt (Sitzung der Berliner 
Gesellschaft fiir Psych, und Nervenkrankheiten, March 11, 
1889). 

Spasms of the muscles concerned here are also unusual. A 
characteristic position of the head is evoked by a unilateral 



342 



DISEASES OF THE SPINAL NERVES. 



spasm of the splenitis capitis (cf. Fig. 106). Bilateral spasm of 
the deep muscles of the neck produces a strong retraction of 
the head, while spasm of the rhomboids alters the position of 
the shoulder-blades, etc. 

Of the nerves belonging to the infraclavicular portion of 
the brachial plexus none is so frequently the seat of disease as 
the continuation of the posterior trunk of the plexus, which 
becomes the musculo-spiral or radial nerve, and supplies the 
skin and the muscles of the extensor surface of the arm. 

The musculo-spiral paralysis can better than any other form 
be recognized at a glance. A patient with paralysis of the 
extensors is unable on stretching out the arm to raise the hand. 




Fig. 107. — Musculo-spiral Paralysis. 



while lateral motion is difficult. Dorsal flexion, which is per- 
formed by the extensor carpi radialis and the extensor carpi 
ulnaris, is impossible, abduction and adduction difficult, the 
hand hangs down flaccidly (" wrist-drop ") (cf. Fig. 107), and 
when rested upon the table can not be raised. On a more 
careful examination it is noticed that the first phalanx of the 
flexed fingers can not be extended without assistance, but that 
if this phalanx is passively extended the patient can straighten 
out the others himself. The first condition is due to the paral- 
ysis of the extensors, which, as is well known, on the dorsal 
surface of the first phalanx pass into an aponeurosis ; the 
second to the preservation of the function of the interossei, 
which are supplied by the ulnar nerve. Since its extensors 
are also implicated, the thumb, of course, can not be actively 



LESIONS OF THE BRACHIAL PLEXUS. 



343 



extended, neither can it be abducted, because the muscles con- 
cerned are also paralyzed. Some interesting conditions will 
be found on examination of the forearm in extension and flex- 
ion. If, for instance, the forearm is extended and pronated, 
supination is impossible, because the supinator brevis is para- 
lyzed. During flexion of the forearm, however, the biceps, 
which is intact, can perform supination without difficult) 7 . If 
the forearm is in a position of supination it is easily flexed by 
the intact muscles, the biceps and the brachialis anticus, while 
if it is half pronated flexion is imperfect, owing to the paral- 
ysis of the supinator longus. The characteristic prominence 
formed by the belly of this muscle when the forearm is flexed 
is absolutely wanting. Any participation of the triceps in the 
paralysis is only observed if the lesion is high up (" crutch 
palsy "). Usually the injury is situated where the nerve turns 
over the humerus or lower down, in which case naturally the 
normal function of the triceps is not interfered with. Perma- 
nent trophic disturbances, shown by pronounced wasting of 
the affected muscles, are rare in cases of pressure paralysis, 
while they are frequent in the paralysis developed as a conse- 
quence and in the course of lead poisoning. 

The flexors, otherwise perfectly healthy, also become weak- 
ened, because their points of insertion are approximated to the 
points of origin more closely than under normal conditions, on 
account of the constant drooping of the hand, and hence the 
interference with motion is aggravated. The patient can hardly 
use the hand at all, he is unable to take hold of anything, the 
finer manipulations necessary for writing, drawing, etc., are 
impossible, and in the majority of cases he is unfit for work or 
for making a living during the whole course of the disease. 

Sensory changes are rarely sufficiently marked to add much 
to his troubles. Sometimes paresthesias may be complained 
of — a feeling of cold, numbness, formication, and the like ; some- 
times, also, there is a distinct decrease of sensibility, so that 
zones of anaesthesia can be made out ; but these changes are 
of relatively small importance, and, as we said, inconvenience 
the patient but little. On the other hand, a source of great 
annoyance is found in the peculiar painless swellings of the 
extensor tendons on the back of the hand. These- node-like 
swellings have been described by Gubler as tenosynovitis hy- 
pertrophica, and are to be attributed to mechanical influences 
acting injuriously on the tendon. 



344 



DISEASES OF THE SPINAL NERVES. 



The duration and course of a musculo-spiral paralysis may 
vary greatly, and it is often hard to give an opinion on these 
points at the very onset of the affection. An electrical exami- 
nation, which reveals the reactions of the muscles and nerves 
to the faradic and galvanic current, is the only means by which 
we can arrive at an opinion as to the duration of the disease. 
The conditions are the same as those we described as existing 
in facial paralysis, and it suffices, therefore, to refer the reader 
to that chapter. But here again be it once more stated a prog- 
nosis should never be given without a previous electrical exam- 
ination of nerves and muscles. 

The aetiology of musculo-spiral paralysis is interesting from 
the fact that it is fairly well understood. While, as all con- 
fess, the cause of most nervous diseases is absolutely unknown, 
and we therefore are forced to fall back on uncertain explana- 
tions, such as exposure to cold, it seems according to our 
present knowledge that musculo-spiral paralysis always can 
be traced back to one of two kinds of causes — viz., mechanical 
or chemical. There are quite a number of lesions due to 
mechanical or traumatic causes. Frequently a man, when 
greatly fatigued, drunk, or exhausted, goes to sleep, using his 
arm, usually the left, as a support for his head ; the latter, 
pressing on the nerve in the lower third of the humerus, gives 
rise to an injury in a relatively short time, or the arm support- 
ing the head of the sleeper may press with its outer side against 
a chair or the like and a paralysis be the result. This is the so- 
called "sleep palsy." Next we have compression happening 
to the patient as a consequence of his daily occupation, due to 
pressure from ropes, handles of water-jars (as in the water- 
carrier paralysis of Rennes, etc.) ; sometimes in infants this 
paralysis occurs from too much compression on the arms by 
too tight swathing-clothes ; sometimes too tight plaster-of-Paris 
bandages have been the cause ; and, finally, all direct injuries 
to the nerve — stab wounds, blows, gunshot wounds, and com- 
pression of the nerve by abnormal callus formation after frac- 
ture of the humerus — must also be mentioned. 

The lesions due to chemical causes may be the result of the 
action of certain poisons, among which lead deserves to be 
mentioned first. It is a fact no less remarkable than well au- 
thenticated, to which we shall again refer when speaking of 
lead poisoning in general, that this agent acts by preference 
on the muscles which are supplied by the musculo-spiral nerve. 



LESIONS OF THE BRACHIAL PLEXUS. 



345 



This musculo-spiral paralysis, however, unlike the form which 
is produced by mechanical action, is not an independent dis- 
ease, but merely a symptom of a general intoxication. Accord- 
ing to the commonly received opinion (Leyden and others), the 
paralysis depends upon a degenerative atrophy of the motor 
peripheral nerve fibres, to which is often superadded a spinal 
affection. It differs in its clinical aspect from the mechanical 
lesion, inasmuch as the supinator longus and the triceps remain 
intact. Of late years several cases have been published where, 
after subcutaneous injections of ether into the extensor surface 
of the forearm for therapeutic purposes, a musculo-spiral pa- 
ralysis appeared (Falkenheim, Arnozan, Remak, H. Neumann, 



M. extensor carpi radialh brcvior 
M. extensor digitorum communis 
M. extensor minimi digiti 
f. extensor indicis 
M. abductor longus pollicis , 
AI. extensor brevis pollicis 
M. extensor longus 

pollicis \ 

\ \ 



Nervus musculo-spiralis jj tricei 
M. brachial™ an tints {e a tern al head 
M. supinator longus 
M. extensor carpi 
radialis longior 
M. extensor carpi 
vlnaris 
M. supina- 
tor brevis 




Fig. 108.— Motor Points of the Musculo-spiral Nerve and the Muscles sup- 
plied by IT. 



cf. lit.). In using the drug in this way this possibility ought to 



In contradistinction to the frequency with which paralysis 
is found, signs of irritation in the distribution of the musculo- 
spiral nerve — that is, spasms — are extremely rare. They have 
especially been observed after manual overexertion — gymnas- 
tics, etc. (Hochhaus, Deutsche, med. Wochenschr., 1886, 47). 

In the treatment electricity not only plays the chief, but the 
only role. From the motor points (Fig. 108) the muscles ought 
to be stimulated with the constant current, and besides this 
frequent extensive applications of the faradic brush to the skin 



346 



DISEASES OF THE SPINAL NERVES. 



of the affected arm ought to be practiced. That the cause, if 
such should be present — for instance, pressure of crutches, of 
dislocated bones, etc. — ought to be removed is self-evident. 
The sensory disturbances which may be found in the distribu- 




tee 

Fig. 109. Fig. no. 

The Distribution of the Cutaneous Nerves of the Arm and Hand. (After 
Eichhorst.) Fig. 109, volar surface of the upper extremity. isc, supraclavicular 
nerve. 2ax, circumflex nerve, ymd, internal cutaneous nerve. 4c/, external cutaneous 
nerve. 5cm, cutaneous medius. 6?ne, median nerve. 7«, ulnar nerve. Fig. no, isc, 
supraclavicular nerve. 2ax, circumflex nerve. 3cps, superior posterior cutaneous nerve. 
y.pi, inferior posterior cutaneous nerve. $cmd, internal cutaneous nerve. 6cm, median 
cutaneous nerve. -jcl, external cutaneous nerve. Sti, ulnar nerve, gra, musculo-spiral 
nerve. lome, median nerve. 



tion of the musculo-spiral we shall mention when considering 
cervico-brachial neuralgia. The mode of distribution of the 
cutaneous nerves of the upper extremity is illustrated in Figs. 
109, 1 10, in. 



The median and ulnar nerves supply together the innervation of 
the muscles and the skin of the inside of the forearm and the hand, 
the former innervating almost all the flexors of the forearm, the 



LESIONS OF THE BRACHIAL PLEXUS. 



347 



pronator radii teres, and the pronator quadratus, the flexor carpi 
radialis, the flexor sublimis digitorum, and a part of the profundus, 
leaving the flexor carpi ulnaris to the ulnar. Among the thenar 
muscles the median supplies the abductor brevis, the opponens, the 
outer head of the rlexor brevis, further, the three first lumbricales, 
while it again leaves to the ulnar, besides the one flexor mentioned, 
the antithenar, the adductor brevis pollicis, the deeper head of the 
flexor brevis pollicis, the fourth lumbricalis, and all the interossei. 

Both nerves have this in common — that they only rarely be- 
come affected by themselves, much more rarely than the mus- 
culo-spiral, and that they are, unlike 
the latter nerve, liable to disturb- 
ances not only in their motor, but 
also in their sensory fibres. We shall 
have to speak, therefore, not only of 
paralyses, but also of neuralgias. 
With regard to the aetiology, we may 
consider it as the rule, just as in mus- 
culo-spiral paralysis, that motor dis- 
turbances only occur as a conse- 
quence of mechanical injury, pro- 
vided there be no other disease pres- 
ent — e. g., progressive muscular atro- 
phy and the like — while neuralgias 
may appear under other circum- 
stances — e. g., after acute diseases, 
after exposure to cold, sometimes also 

without any demonstrable cause. The ulnar paralysis may be 
caused by certain occupations, as Duchenne has already ob- 
served repeatedly in workingmen who are obliged to press the 
elbow firmly upon a hard surface. It is not a rare occurrence in 
those who have to use the ulnar side of the hand — hypothenar 
eminence— a great deal to strike certain instruments (cabi- 
net-makers, dyers, cobblers, etc.). 

A pure median paralysis is chiefly characterized by the in- 
ability to pronate the forearm and to flex the hand, as we can 
easily understand from the anatomy of the parts. A very 
slight flexion of the hand toward the ulnar side is, however, 
rendered possible by the action of the intact flexor carpi ul- 
naris. The terminal phalanges can not be bent, but in the first 
phalanges, which are under the control of the interossei, this 
motion is not impaired. The part of the flexor profundus digi- 




Fig. in. — Distribution of the 
Sensory Nerves on the Back 
of the Fingers (Krause). ;-, 
musculo-spiral nerve, u, ulnar 
nerve, m, median nerve. 



348 



DISEASES OE THE SPINAL NERVES. 



torum which is supplied by the ulnar makes it possible for the 
patient to seize some objects with the third, fourth, and fifth 
fingers. The extended and adducted thumb, which lies in 
close apposition to the index finger, is as good as useless. 

On the other hand, we find in ulnar paralysis that the 
thumb can not be pressed against the index finger on account 
of the paralysis of the adductor pollicis, that the terminal 
phalanges of the fingers can not be straightened, the first ones 
not flexed (paralysis of the interossei), and that the little finger 
is almost wholly useless. With the median paralysis the ulnar 




Fig. 112. — Motor Points of the Median Nerve and the Muscles supplied by it. 



form has this in common, that flexion at the wrist joint is great- 
ly impaired. In the latter especially lateral movement toward 
the ulnar side is interfered with owing to the paralysis of the 
flexor ulnaris. Lastly, the difficulty which is experienced by 
the patient in spreading his fingers apart and bringing them 
together again, movements which are indeed almost impossi- 
ble, greatly facilitate the diagnosis of ulnar paralysis, which, 
however, for that matter, is always simple. 

Muscular atrophies not uncommonly develop in both of 
these paralyses, but more frequently in the ulnar form. The 
interosseal spaces on the back of the hand become sunken in, 
and, if the wasting affects chiefly the interossei and the lumbri- 
cales, the hand assumes a peculiar appearance. It becomes 
not unlike a claw, since the healthy antagonists — the extensor 
digitorum communis and the flexor digitorum — produce a dor- 
sal flexion of the first phalanges and a complete palmar flexion 



LESIONS OF THE BRACHIAL PLEXUS. 



349 



of the second and third (cf. Fig. 115). This is called the " claw 
hand," the " main en griffe" of the French. 

Atrophy confined to the antithenar eminence I have repeat- 
edly observed in cabinet-makers. They themselves attribute 
it to the continued use of the plane. 

The affections of the sensory fibres of the median and ulnar 
nerves may either occur alone or be found associated with 
those of the motor fibres. In the latter case we have to contend 
with disturbances of sensibility, parassthesias, numbness, anaes- 
thesia, and pains, sometimes quite well pronounced, which es- 
pecially appear in the initial stage of the paralysis. In the 
former there are genuine neuralgias, acute, spontaneous, lanci- 
nating pains which follow the course of the nerve and which 
are intensified by pressure upon it. Such pains are more fre- 
quently observed in the distribution of the median than in that 




M. flexor carpi ulnaris 

Fig- 113- 



M. Ivmbri- 

cales III et IV 

M. opponens min. dig. 

M. flexor minimi digiti 

M. abductor minimi digiti 

M. palmaris brevis 

Ken us ulnaris 



of the ulnar, but they are not common in either of these 
regions. I have known them to occur occasionally after acute 
diseases, especially after typhoid fever. In their course they 
differ in no way from other neuralgias. The only fact remark- 
able is that atrophy of the interossei and the " claw hand " 
may develop in their course even when there are no motor 
disturbances present. A relapse in a case of ulnar neuralgia 
may occur after an interval of years, but no satisfactory ex- 
planation for this has been discovered. 

Lastly, we have to consider in the upper arm the musculo- 
cutaneous and the circumflex nerves (Fig. 116), either of which 



35o 



DISEASES OF THE SPINAL NERVES. 



may be affected by itself or in connection with other nerves of 
the plexus. The former supplies the coraco-brachialis, the 
brachialis anticus, and biceps ; the latter, the deltoid. 

Lesions of the motor fibres of the musculo-cutaneous, which 
are only met with independently after injury due to surgical 
operations, impair and completely prevent flexion of the fore- 
arm on the upper arm. In lesions of the circumflex, motion 
of the arm away from the trunk is difficult, and even ren- 
dered impossible, if, as often happens in the course of the 
disease, the deltoid atrophies. This atrophy is readily recog- 
nized by the flattening of the shoulder, and is often associated 
with reaction of degeneration. Occasionally the participation 




M, abductor minimi digiti 



M. interossei I— IV 



Fig. 114.— Motor Points of the Ulnar Nerve. 



of the sensory fibres of the circumflex is more prominent ; the 
patients then complain of violent neuralgic pains (Heon, cf. 
lit.), which are aggravated if any attempt is made to move the 
arm. It is important in such cases to make a careful exami- 
nation of the shoulder joint, and frequently we shall find a 
chronic inflammation here to be the cause of the neuritis. 

In other cases, again, we can not make out any organic 
changes in the joint, and we have to think of a joint neurosis. 
For information on this point the reader is referred to the 
chapter on hysteria. A severe concussion, a fall upon the 
shoulder, which at first produces hardly any symptoms, may 
give rise to disease, lasting for years, in which both the joint 
and the nerves of the plexus take part. 

In any one of these affections of the nerves of the arm we 



LESIONS OF THE BRACHIAL PLEXUS. 



351 



should in the treatment, besides aiming at the removal of the 
cause if such be found, make use as soon as possible of the gal- 
vanic current. It is a mistake to lose time with other meas- 
ures, such as bathing, massage, rubbing, and the like. Where 




Fig. 115.— Claw-hand. (After Duchenne.) 



the electrodes are to be applied may be learned from Figs. 
108 to 116, where the motor points are accurately given. We 
need hardly say that, besides the electricity, various placebos, 
rubbing and passive motion, may be used to quiet the patient's 
mind. 

Not uncommonly several nerves of the brachial plexus are 
paralyzed at the same time. Duchenne was the first to de- 
scribe such instances in children in consequence of obstetrical 

N. musculo cutanevs 

M. brachicdis anficus 
M. biceps brachii 




Fig. 116.— Motor Points of the Musculo-cutaneous Nerve and the Muscles 

SUPPLIED BY IT. 

operations, such as version and subsequent extraction, the 
Prague method of extraction, etc., and designated this form as 
"paralysie obstetricale infantile du membre superieur," or 
birth palsies. Independently of the French investigator, Erb 



352 



DISEASES OE THE SPINAL NERVES. 



has given us an excellent well-defined picture of such a paral- 
ysis. The lesion which affects the plexus gives rise to a simul- 
taneous paralysis of the deltoid, the biceps, the brachialis 
anticus, and the supinator longus, and the patient can neither 
move his upper arm away from the body, nor approach the 
forearm to the upper arm. The whole extremity hangs down 
flaccid, while the fingers and hand retain their mobility. The 




Phrenic nerve 



Anterior thoracic 
nerve (M. pector.) 



Brachial plexus 



ErUs supraclavicular point 
Fig. 117. 



lesion in such cases must be situated at a point where the cir- 
cumflex and the musculo-cutaneous and the musculo-spiral are 
still close together — i. e., at about the exit of the sixth cervical 
nerve — between the scaleni, and it is from this so-called 
" Erb's " or " supraclavicular " point (cf. Fig. 117) that we are 
able to stimulate simultaneously all these four above-mentioned 
muscles. If the infraspinatus is also taken in, the arm is in a 
position of internal rotation, and can not be turned outward. 

This paralysis, which Erb has aptly termed "combined 
shoulder-arm palsy," is often a very tedious and troublesome 



LESIONS OF THE BRACHIAL PLEXUS. 



353 



affection. The longer it lasts the more the nutrition of the 
muscles suffers, and the most varied degrees of atrophy, which 
is often especially marked in the deltoid, are seen. On elec- 
trical examination we find that the faradic and galvanic excita- 
bility of the nerves, although not completely lost, is diminished, 
as is also the faradic excitability of the muscles, while the gal- 
vanic excitability of the same has undergone qualitative as 
well as quantitative changes, a condition which Erb has desig- 
nated as partial reaction of degeneration. Sometimes, also, 
there is present complete reaction of degeneration (cf. page 
91). If the sympathetic is also implicated (Seeligmiiller), the 
ensuing paralytic symptoms, contraction of the pupil, narrow- 
ing of the palpebral fissure, and retraction of the bulb on the 
affected side, are further sources of annoyance to the patient. 
How the participation of the sympathetic is to be explained, 
whether, as Klumpke (cf. lit.) holds, by a lesion of the commu- 
nicating branch of the first dorsal, we can not decide. If the 
sensory fibres are also implicated, the patient complains, in 
addition to the motor, also of sensory disturbances, not only of 
great difficulty in moving the arm, but also of pains, numbness, 
and formication. 

The treatment, of course, consists in the use of electricity, 
galvanic stimulation from Erb's point, and the application of 
the faradic brush, which, acting reflexly, often give very good 
results. 

Peculiar and very curious motor phenomena in the upper 
extremities are observed in connection with and as a direct 
consequence of certain callings. Such occur in cases where no 
particular exertion of the muscles might lead us to think of a 
peripheral lesion of the plexus as the result of overstrain, but 
in those whose occupations bring into play complex, co-ordi- 
nated movements. Since in many cases — but by no means in 
all — a faulty co-ordination of the movements is the cause of the 
affection, we may for the present accept the name of "co-ordi- 
nation occupation neurosis," which was proposed by Benedikt, 
at the same time insisting upon the fact that it only fits a cer- 
tain small number of cases. 

Among the occupations which relatively frequently give 
rise to the disturbance in question the most important certainly 
is writing, and writer's cramp — mogigraphia, graphospasmus — 
is one of the nervous diseases to which most careful study has 
been devoted. Nevertheless, our knowledge is extremely 
23 



354 



DISEASES OF THE SPINAL NERVES. 



limited, and we must confess that we have not as jet gotten 
beyond the description of the symptoms. The pathogenesis 
and therapeutics are terrce incognita. 

In the first place, we ought to state that only in a fractional 
number of cases have we to deal with a cramp or spasm ; more 
often the conditions are the following : The patient, after having 
for weeks, perhaps months, noticed that while writing the hand 
becomes tired more easily than before, finds one day that he is 
utterly unable to write another line without great strain ; as 
soon as the pen is taken into the hand the sensation of fatigue 
comes on; hand and arm drop as if paralysed, while at the 
same time the patient may complain of more or less intense 
pain in the forearm, upper arm, and possibly in the shoulder. 
The writer's cramp in such cases is in reality a writer's paral- 
ysis. In other instances, as soon as the penholder is clasped, 
the hand begins to tremble and the handwriting becomes un- 
certain and tremulous, which is all the more striking because 
on examination the patient's hand, especially the right, proves 
to be quite steady if it is not used in writing. Sometimes there 
is an actual spasm when the penholder is seized, which attacks 
the muscles of the hand as well as those of the forearm, so that 
hand and arm make involuntary movements or they become 
stiff and immobile (clonic and tonic spasm). The pen is either 
irregularly jerked to and fro or firmly pressed against the 
paper — in both cases writing is absolutely impossible. On 
further examination nothing else is discovered, and what is 
more especially interesting, the patient is able to do anything 
else with his hands, even the finest work. He is able to draw 
(with a pencil), play the piano, etc. ; moreover the electrical 
examination of the apparently seriously affected muscles sel- 
dom reveals anything abnormal worthy of mention — Dubois 
(Schweiz. Correspond. Blatt, 1887, 5) found the excitability for 
both currents, especially in the thenar muscles, increased. 
Sensibility is, on the whole, normal. Pains only occur on 
forced attempts to write ; in short, the patient can do anything 
demanded of him except write. 

Analogous to the affections just described are the condi- 
tions of fatigue in the muscles of people, chiefly professionals, 
who play the piano a great deal. In them not only the right 
hand, but, especially in female patients, the left also is affected. 
Pain and weakness may become so marked in both hands that 
piano-playing has to be given up completely. This becomes 



CO-ORDINA riON—OCCUPA TION— NEUROSES. 



355 



the more necessary when the symptoms persist during- rest as 
well, and not only when the patient is playing. Such disturb- 
ances are also noted in telegraph operators, cigar-makers, 
dairy-maids (as the result of milking cows) ; also, but rarely, in 
tailors it is produced by the frequent handling of the heavy 
shears, etc. In all cases it is evident that the occupation is 
the sole cause, although we do not know how and upon what 
organs it acts injuriously. It is very unlikely that the disturb- 
ance is of a peripheral nature, the negative result of the exam- 
ination of muscles and nerves and the uselessness of any treat- 
ment seeming to indicate this. We can not accept either the 
theory which attempts to explain the symptoms by a primary 
weakness of certain muscles and a secondary spasm of the an- 
tagonists (Zuradelli), or that which assumes the spasm to be of 
a reflex nature, starting from the sensory nerves of the skin 
(Fritz) ; or, finally, the explanation that we have to deal with a 
disturbance in conduction of the nerve muscle apparatus used 
in writing ; but we are rather of opinion that the weakness and 
the motor disturbances of the upper extremity arising in con- 
sequence of the occupation are of a central nature and are to 
be referred to the brain cortex. The situation of the centres 
concerned in writing and in other movements which depend 
upon a co-ordinated action of the muscles of the hands is un- 
known. These centres in consequence of overexertion, but also 
often without any appreciable cause, are thrown into a state of 
paralysis or irritation which gives rise to corresponding dis- 
turbances in the extremities. Perhaps this may at times arise 
simply as the result of a general increased nervousness which 
may have a hereditary origin. It is evident that besides those 
affections which are due to a functional disturbance of the cor- 
tex there are those in which anatomical lesions, whether of the 
central organs or of the peripheral nerves, may be the cause of 
the same symptoms as those now under consideration. Thus 
we may sometimes meet with cases of old almost cured hemi- 
plegias in which as the only remaining disturbance a slight 
difficulty in writing or similar occupations may be present. 
The same may happen in slight disseminated scleroses of some 
collections of fibres in the spinal cord, or, finally, as I have had 
occasion to observe repeatedly, in the initial stage of tabes, and 
the disturbance at the first glance may suggest to us writer's 
cramp. Hence we should, first of all, endeavor to decide 
whether the trouble is an independent affection or whether 



356 



DISEASES OF THE SPINAL NERVES. 



it is to be regarded merely as a symptom of an underlying 
disease. 

The prognosis is usually unfavorable. Only in the rarest 
instances are we able to afford the patients any decided last- 
ing relief, a fact of which we should inform the friends before 
taking charge of the case. Only when we are able to get hold 
of the patient in the earliest stages of the trouble and can in- 
sure him perfect rest and the removal of the exciting cause, 
such as writing, piano-playing, telegraphing, etc., for weeks and 
months, is it sometimes possible to effect an absolute cure. If 
this can not be done, and if the rest is not complete, the success 
of all our attempts becomes very uncertain and the result will 
usually be disappointing. We may try massage, as has been 
done also by some non-professional specialists with transient 
success. Galvanism, faradism, rubbing with different external 
applications, hydrotherapy, gymnastics, may be advised. The 
result is usually the same as if strychnine or atropine is in- 
jected hypodermically or if the different nervines be given inter- 
nally for months. Writing may be facilitated by using a pen- 
holder passed through a potato or through a wooden ball fitted 
to the hollow of the hand, or by using Nussbaum's bracelet. The 
advice to educate the left hand to write is always good because 
it gives the right hand a rest. Yet the value is by no means 
lasting, because the motor disturbance, as a rule, shows itself 
soon in that hand also, a fact which is an additional argument 
in favor of the central nature of the disease. 

The simultaneous affection of several sensory nerves of the 
brachial plexus, analogous to the motor disturbance in the 
shoulder-arm palsy, is not common. When it does occur the 
pains are very violent and deprive the patient of the use of 
the extremity. The cervico-brachial neuralgia may affect all 
the sensory branches of the brachial plexus, so that the whole 
upper arm, forearm, and hand are painful ; but it may also be 
confined to the area of distribution of one nerve, often the 
musculo-spiral or median. 

Painful points can sometimes be demonstrated in the region 
of the circumflex nerve over the scapula, of the median in the 
bend of the elbow, of the musculo-spiral in the lower third of 
the humerus, and of the ulnar at the internal condyle. Vaso- 
motor and trophic changes may be entirely absent, yet the 
skin of the fingers not rarely looks glossy and atrophic (" glossy 



LESIONS OF THE BRACHIAL PLEXUS. 



357 



fingers"). Here, again, traumatism, mechanical pressure — by 
tumors, aneurisms, etc. — are the most prevalent causes of the 
neuralgia. It may occur reflexly after amputation of the 
fingers or the forearm. A bilateral neuralgia of this kind is 
suggestive of a spinal disease, more especially of pachymenin- 
gitis cervicalis hypertrophica. 

The treatment is in the main the same as in other neural- 
gias. Besides narcotics the electrical treatment should be be- 
gun as soon as possible. Descending currents through the 
diseased nerve, as well as the application of the anode over the 
affected plexus, are to be recommended. The faradic brush is 
usually borne well and is of use, although the manipulation 
itself may not be very agreeable to the patient. In rare in- 
stances we must have recourse to energetic counter-irritants to 
the skin. We have repeatedly made very successful use of the 
points de feu with Paquelin's cautery. 

Paraesthesias and anaesthesias are quite common in the dis- 
tribution of the brachial plexus. They are not always con- 
fined to one nerve, Upper arm and forearm, the hands also, 
are frequently affected, particularly when the occupation ne- 
cessitates overexertion of them — e. g., in brick-makers. Again 
they are caused by the action of cold and hot water, often also 
by water containing lye (anaesthesia lavatricum, and the mal 
des bassins of the women engaged in unwinding the silk from 
the cocoons in the silk-spinning mills, etc.). For such patients 
the only remedy lies in abstention from this kind of work. 



LITERATURE. 

Lesions of the Cervical Plexus. 

Peter, M. Neuralgia phrenica. Arch. g£ner., 1871, 6me ser., xvii, p. 303. 
Erb. Handbuch der Krankheiten des Nervensystems. 2. Aufl., 1876, ii, pp. 

124, 125. 
Striimpell. Loc. cit., 1887, p. 32. 
Eichhorst. Loc. cit., 1887, pp. 47, 79, 82. 

Lesions of the Brachial Plexus. 
1. Paralysis of the Serratus. 

Berger, O. Die Lahmung des Thoracicus longus. Habilitationsschrift, Bres- 

lau, 1873. 
Bruck. Ein Fall von Serratuslahmung nach acuter Krankheit (Typhoid). In- 

aug. Dissert. Vratisl., 1873. 



358 



DISEASES OF THE SPINAL NERVES. 



Lewinski. Ueber die Lahmung des Serratus anticus major. Virchow's Archiv, 

1878, lxxiv, 4, p. 473. 
Lewinski. Zur Diagnose der Serratuslahmung. Virchow's Archiv, 1881, lxxxiv, 

1, p. 71. 
Baumler. Isolirte Lahmung der Serrat. ant. maj. Arch. f. Psych, und Nerven- 

krankheiten, 1882, xiv, 3, p. 722. 
Dixon, Mann. Serratus Paralysis. Lancet, February, 1884, i, 5, 6. 
Hoffmann. Isolirte periphere Lahmung des Nerv. suprascapul. sinister. Neurol. 

Centralbl., 1888, 9. (Pains and atrophy of the muscles supplied by the 

nerve.) 

2. Musculo-spiral Paralysis (not including the Saturnine Form). 

Fischer. Zur Lehre von der Lahmung des N. radialis. Deutsches Arch. f. klin. 

Med., 1876, xvii, 4, 5, 392. 
Onimus. Gaz. hebdom., 1871, 2me ser., xv, 25. 
Whitson. Musculo-spiral Paralysis in Consequence of Pressure exerted by a 

Piece of Bone. Edinb. Med. Journ., 1882, xxvii, p. 724. 
Boyer. De la paralvsie du nerf radial par compression tempo raire. These de 

Paris, 1883. 
Joffroy. Du role de la compression dans la production de la paralysie radiale. 

Compt. rend, gener.. May 14, 1884, p. 284. 
Arnozan. Gaz. hebd., 1885, xxxii, 2, 3. — E. Remak. Berl. klin. Wochenschr., 

1885, xxii, 5.— H. Neumann. Neurol. Centralbl., 1885, iv, 4. — Falkenheim. 

Mittheilungen aus der med. Klinik zu Konigsberg, 1888. (Musculo-spiral 

paralysis after subcutaneous injection of ether.) 
Vulpian et Dejerine. Recherches cliniques et experimentales sur la paralysie 

radiale. Compt. rend. hebd. de la Soc. de Biol., 1886, 15, p. 187. 
Scheiber, H. Ein Fall von schwerer complicirter Schlaflahmung am linken 

Arme. Neurol. Centralbl., 1886, v, 15. 
Kobner, H. Ein Fall von gleichzeitiger traumatischer (Druck) Lahmung der 

Nervi radial., uln. und median, sinistr. Deutsche med. Wochenschr., 1888, 

10. 
Gluck. Sitzung der Berliner Gesellschaft f. Psych, u. Nervenkrankheiten vom 9. 

Juli 1888. (Traumatic musculo-spiral paralysis cured by secondary nerve 

suture.) 

3. Median and Ulnar Paralysis. 

Bernhardt. Ueber den Bereich der Sensibilitats-Storung an Hand und Finger 

bei Lahmung des Medianus, sowie zur Pathologie der Radialisparalysen. 

Arch. f. Psych, und Nervenkrankheiten, 1875, v, 2. 
Tilden. Trophoneuroses after Injury to the Median Nerve. New York Med. 

Record, September 11, 1886, xxx, p. 30, 4. 
McNaught. Ulnar Neuralgia. Brit. Med. Journ., April 30, 1887, p. 933. 
Poore. Lancet, September, 1882, ii, 10, 12. 
Leudet (de Rouen). Gaz. m£d. de Paris, September 15, 1883. 
Hess, Julius. Ueber Temperaturen und deren Messung bei Ulnarislahmungen. 

Berl. klin. Wochenschr., 1886, xxiii, 30. 
Ballet, G. Accidents consecutifs a la compression habituelle du cubital chez un 

ouvrier employe a ouvrager le verre. Revue de med., 6, 1885. 



LESIONS OF THE BRACHIAL PLEXUS. 



359 



Philiotis. De la n£vrite peripherique du cubital consecutive a la fievre typhoide. 

These de Paris, 1885, No. 119. 
Eulenburg. Ueber Lahmung durch polizeiliche Fesselung (Arrestantenlahm- 

ung) der Hand. Neurol. Centralbl., 1889, 4. 
Rieder. Medianus-Neuritis. Miinchener nied. Woch., 12, 1889. 

4. Musculo-Cutaneous and Circumflex Paralysis. 

Heon. De la nevralgie circonflexe ou axillaire. These de Paris, 1882, No. 277. 
Fauvel. Des paralysies traumatiques d'origine peripherique. These de Paris, 

1885, No. 371. 
Paradeis. Zur Diagnose und Prognose der Axillarislahmung. Miinchn. med. 

Wochenschr., 1888, 21, 22. 

5. Plexus Paralyses— Combined Shoulder-arm Palsy. 

Seeligmuller. Zur Pathologie des Sympathicus. Deutsches Arch. f. klin. Med., 

1877, xx, p. 101. 
Bernhardt. Beitrag zur Lehre von den Lahmungen im Bereiche des Plexus 

brachialis. Zeitschr. f. klin. Med., 1882, iv, 3, p. 415. 
Vierordt. Zwei Falle von der Form der "combinirten Schulterarmlahmung." 

Neurol. Centralbl., 1882, 13. 
Morvan. On Paralysis of the Arms, with Analgesia and Panaritia. Gaz. hebd., 

2me s6r., 1883, xx, 35, 36, 38. 
Klumpke. Contribution a l'etude des paralysies radiculaires du plexus brachial. 

Revue de med., Juillet-Sept., 1885. 
Martius. Berl. klin. Wochenschr., 1886, No. 28. 
Nonne. Deutsches Arch. f. klin. Med., 1886, Bd. 40, p. 62. 
Rose. Deutsche Zeitschr. f. Chirurg., 1886, Bd. xxiv, p. 392. 
Vinay. Paralysies radiculaires superieures du plexus brachial, d'origine profes- 

sionelle. Lyon m£d., 53. 1886. 
Rendu. Revue de mdd., 1886, p. 737. 
Dufourt. Lyon m6d., 1886, No. 4. 
Bernhardt. Neurol. Centralbl., 1886, 6, p. 141. 
Rose. Deutsche Zeitschr. f. Chirurg., 1886, xxiv, 3, 4. 
Stadelmann. Neurol. Centralbl., 1887, 17. 
Nonne. Deutsche med. Wochenschr., 1887,46. 
Muralt. Einige, zum Theil chirurgische Lahmungen im Bereiche des Plex. 

brachialis. Schweiz. Correspondenzbl., 1888, xviii, 15. 
Clutton. Lancet, November 17, 1888, p. 962. 
Remak, R. Article on " Radialislahmung " in Eulenburg's Real-Encyclopadie. 

2. Aufl. Wien und Leipzig, 1888. 
Middeldorpf. Wiener med. Wochenschr., 1888, 14. (Pressure palsy of the 

musculo-spiral and ulnar nerves.) 

6. Co-ordination Occupation Neuroses. 

Napias. Photographer's Cramp. Revue d'Hygiene, November, 1879. 
Mobius. Berl. klin. Wochenschr., 1880, xvii, 21. (Cramp in consequence of 

playing the zither.) 
Dally. Journ. de Therapeut., 1882, 3, 4. 



360 DISEASES OF THE SPINAL NERVES. 

Robinson. Cases of Telegraphist's Cramp. Brit. Med. Journ., November, 1882. 

Poore. Brain, 1883, p. 233. (Sawyer's Cramp.) 

Vigouroux. Progr. med., 1882, x, 3. 

Nussbaum. Bayer, arztl. Intelligenzbl., 1882, xxix, 39. (Description of the 

bracelet.) 
Villemin. Arch, de med. et de pharm. milit., 1883, pp. 91-95. 
Poore. A Case of Hammerman's Cramp. Lancet, August 21, 1886, 8. 
Lallemand. De la crampe des ecrivains et son traitement. These de Paris, 

1887. 
Poore. The Lancet, 1887, 3322. (Writer's Cramp.) 
Gaborian. Contribution a letude des spasmes professionels. These de Paris, 

1887. 
Poore. On Certain Conditions of the Hand and Arm which Interfere with the 

Performance of Professional Acts, especially Piano-playing. Brit. Med. 

Journ., February 26, 1887. 
Zenner. Berliner klinische Wochenschr., 1887, 17. 
Chambard. Contribution a l'etiologie et a la symptomatologie des impotences 

fonctionelles. Revue de med., 1887, vii, 6, p. 464. (Occupation neuroses.) 
Henschen. Writer's Cramp. Upsala laekare forenings. Forhandling, 1888. 
Richet. Contributions aux paralysies et aux anesthesies reflexes. Arch, de 

Physiol, norm, et Pathol., 1883, 7. 
Turbert. Contribution a l'etude des nevralgies du membre superieur. These 

inaugur. Paris, 1884. 
Coster. Zum Capitel der Arbeitsparesen. Berl. klin. Wochenschr., 1884, 826. 
Squire, J. Edward. Some Cases of Local Numbness of the Extremities, with 

a Comparison between Local Syncope and Night Palsy. Lancet, Decem- 
ber, 1885, ii, 23. 
Bernhardt. Ueber eine weniger bekannte Neurose der Extremitaten besonders 

der oberen. Centralblatt fur Nervenheilkunde, 1886, ix, 2. 
Remak. Zur Pathologie des Melkerkrampfes. Deutsche med. Wochenschrift, 

1889, 13, p. 158. 

II. Diseases of the Dorsal Nerves. 

The anterior (ventral) divisions of the twelve dorsal nerves are 
called the intercostal nerves, since they run in the intercostal spaces. 
They supply the intercostal muscles, the levatores costarum, the 
serrati postici, and the three broad abdominal muscles. To the in- 
tegument of the chest and abdomen they supply cutaneous branches. 
The posterior divisions of the dorsal nerves are divided into internal 
and external branches. The former are distributed to the deep 
muscles of the back, sending nerves to the rhomboidei and the latis- 
simus dorsi ; the latter, passing between the longissimus dorsi and the 
sacrolumbal, also furnish numerous muscular branches, and, to- 
gether with the internal, supply the skin of the back as far down as 
the crest of the ilium. 

The sensory as well as the motor fibres of the dorsal nerves 
may become the seat of disease, but, and this is practically of 



DISEASES OF THE DORSAL NERVES. 361 

much importance, the anterior, the intercostal nerves, are more 
subject to sensory disturbances, while the diseases of the pos- 
terior branches are almost exclusively motor affections. 

The disease of the anterior branches, the so-called intercos- 
tal neuralgia, is found with relative frequency in the female 
sex, especially in those of middle age. iEtiologically, oc- 
cupation and hard work in general are of some importance. 
Servant girls and women of the poorer classes suffer more 
frequently than others. I have seen many such instances, and 
have found it besides in the course of phthisis pulmonalis when 
associated with peripheral neuritis. Traumatism, aortic aneu- 
rism, and spinal affections, may also give rise to intercostal 
neuralgia. 

The pain appears in paroxysms and attacks more frequently 
the left than the right side, and almost exclusively the anterior 
or lateral, rarely the posterior portion of the nerve trunks. It 
often follows the course of the nerve and at times reaches a 
degree of intensity most distressing to the patient. The re- 
spiratory movements, more especially coughing and sneezing, 
cause great agony. Three tender points can usually be demon- 
strated — one close to the vertebral column, one in the middle 
of the course of the nerve, and one close to the sternum — 
called respectively the vertebral, lateral, and sternal points. 
The fact that frequently after cessation of the pain a herpes 
zoster appears is of great interest, although the question 
whether we have to regard the latter as a genuine trophic dis- 
turbance or simply as an extension of the inflammation from 
the nerve endings to the skin, as Dubler thinks, is still unset- 
tled. For the prognosis it is without significance. In all cases 
of intercostal neuralgia the prospect for complete recovery is 
slight. Although we may succeed sometimes in cutting short 
the individual attacks, we can never be certain that they will 
not recur, and there are persons who all their life long are 
condemned to suffer from this disease. 

The diagnosis is not always simple. Rheumatism of the 
chest muscles can easily be taken for intercostal neuralgia, and 
vice versa. In such cases we shall find it useful to observe 
whether motion has any influence on the pain or whether this 
exists independently. If there is a history of traumatism, neu- 
ritis is always to be thought of, only we must beware of being 
deceived by malingerers, and to avoid this the condition of the 
abdominal reflex and the pupil should be examined into. The 



362 DISEASES OE THE SPINAL NERVES. 

former in the case of neuritis is increased, the latter often di- 
lated on the side of the pain. This fact was first established 
by Seeligmiiller, and shows that the sympathetic is often im- 
plicated here just as in the affections of the brachial plexus 
(Deutsch. med. Wochenschr., 1887, 45). 

In the treatment morphine plays the most important role, 
and, as a matter of fact, it is of much more value than the much- 
lauded subcutaneous injections of osmiumine (one syringeful 
of a one-per-cent solution at a dose), for this not only fre- 
quently disappoints 'us, but also produces local troubles, small 
abscesses, etc., so that the patient is left almost in a worse con- 
dition than before. The faradic brush, the "points de feu " 
with Paquelin's cautery, blisters applied to the painful points, 
may be tried ; but, on the whole, these means effect but little. 

Among the intercostal neuralgias, the so-called mastodynia 
(the irritable breast of Cooper), a neuralgia of the mamma, is 
to be included. This is a not very frequent affection of the 
female after puberty and may be connected with lactation. It 
is a very painful and distressing trouble, against which usually 
all remedies are tried in vain, so that in desperate cases the 
patient herself suggests amputation of the breast to get rid of 
the dreadful suffering. The aetiology is obscure. Traumatism 
is rarely the cause. Ill-fitting corsets may have some influence, 
but women with well developed and those with small breasts 
are equally liable to the affection. The hyperassthesia of the 
skin often hinders a careful examination by palpation. With 
the tips of the fingers we should endeavor to determine 
whether there are hard nodules in the tissue, which to the in- 
experienced often suggest beginning carcinoma. In some 
cases my patients have derived some transient benefit from 
suspension of the breast and the application of hot cloths. 
Here also morphine is indispensable (cf. Terrillon, Des neu- 
ralgies du sein ; Progr. med., 1886, xiv, 10). 

The motor disturbances affecting the muscles of the back 
supplied by the posterior branches of the dorsal nerves are 
generally paralyses. We are far from being familiar with the 
symptoms of the affections of every one of these muscles, and 
must content ourselves for the present with mentioning the 
paralysis of the erector spinas, the sacro-lumbalis, and the lon- 
gissimus dorsi, which may be affected in the lumbar, dorsal, 
or cervical portion of the vertebral column. Bilateral paraly- 



DISEASES OF THE DORSAL NERVES. 



363 



sis causes curvature of the spine backward (kyphosis), unilat- 
eral paralysis lateral curvature (scoliosis). Paralysis or pare- 
sis of the erectors in the lumbar region gives rise to a 
characteristic walk and a characteristic position of the body. 
The upper part of the body is bent strongly backward, so 
that the lumbar part of the vertebral column is markedly 
curved forward. If by any movement the upper part of the 
body is brought forward so that its centre of gravity is no 
longer behind that of the whole body, the patient falls forward, 
or, if the patient sits on the floor, he has the greatest difficulty 
in getting up. The manner in which he raises himself is so 





Fig. 120. Fig. 121. 

Figs. 118-121 illustrate the manner in which a child whose erectores spina; are paralyzed 

gets up from the ground. (After Gowers.) 

characteristic of paralysis of the erector muscles that we have 
represented it in Figs. 118 to 121. The patient first gets upon 
all fours, and then climbs, as it were, with his hands up his own 
legs, constantly endeavoring to bring the upper part of the 
body as far back as possible by movements in the shoulders 
and the arms so that the abdominal muscles may resume the 
duty of balancing the body. This mode of getting up can best 
be studied in pseudo-hypertrophic paralysis. 

III. Diseases of the Lumbar Nerves. 

The posterior lumbar nerves are, like the dorsal, divided into 
outer and inner branches, which are distributed to some of the mus- 



3 6 4 



DISEASES OF THE SPINAL NERVES. 



cles of the back and the skin of the lumbar and gluteal region. The 
anterior, by far the stouter, are connected each with the correspond- 




Fig. 122. — Diagrammatic Outline of the Lumbar and Sacral Plexuses. D XII, 
last dorsal nerve. L I- V, the five lumbar nerves. S I- V, the five sacral nerves. CI, 
the coccygeal nerve, r, ilio-hypogastric nerve, i', ilio-inguinal nerve. 2, genito-cru- 
ral nerve. 2', external cutaneous nerve of the thigh, crur, anterior crural nerve, obt, 
obturator nerve. 3, superior gluteal nerve, sc, great sciatic nerve. 4, small sciatic 
nerve. 4', inferior gluteal nerve. 5, inferior pudendal nerve. 5', posterior cutaneous 
nerve of thigh and leg. 6, 6, braach to obturator internus and gemellus superior. 6', 6', 
branch to the gemellus inferior, quadratus femoris, and hip joint. 7, twigs to the pyri- 
formis. 8, pudic nerve. 9, visceral branches. 9', twig to the levator ani. 10, perforat- 
ing cutaneous nerve, n, coccygeal branches. 



LESIONS OF THE LUMBAR NERVES. 



365 



ing ganglion lumbale of the sympathetic. They form the lumbar 
plexus which lies behind and in the psoas muscle. Its branches are 
(Fig. 122) : (1) The ilio-hypogastric nerve, for the transversalis and 



ii( """V>. 



i d 



li i, 



m 1 \ 



\ok / 



s 



\ st VJ I 




li 
pep sc 

Fig. 123. Fig. 124. 

Areas of Distribution of the Cutaneous Nerves of the Lower Extremity. 
(After Henle.) Fig. 123, anterior surface. 1, middle cutaneous nerve. 2, external cu- 
taneous nerve. 3, ilio-inguinal nerve. 4, genito-crural nerve. 5, external speimatic. 
6, posterior cutaneous nerve. 7, obturator nerve. 8, internal saphenous nerve. 9, com- 
municating peroneal. 10, superficial peroneal, n, deep peroneal. 12, communicating 
tibial. Fig. 124, posterior surface. 1, posterior cutaneous nerve. 2, external cutaneous 
nerve. 3, obturator nerve. 4, median posterior femoral cutaneous. 5, communicating 
peroneal. 6, saphenous nerve. 7, communicating tibial. 8, pkntar cutaneous. 9, 
median plantar nerve. 10, lateral plantar nerve. 



the internal oblique; (2) the ilio-inguinal, for the skin of the pubes 
and the genitals (N. scrotales et labiales anteriores) ; (3) the genito- 
crural, which divides into the external spermatic or genital branch 
and the lumbo-inguinal or crural branch, the former supplying the 
spermatic cord, the cremaster muscle, and the testis, the latter the 



3 66 



DISEASES OF THE SPINAL NERVES. 



skin in the inguinal region ; (4) the external cutaneous, for the skin 
down to the knee; (5) the obturator, which gives off a posterior 
branch to the obturator ext. and. adductor magnus and an anterior 
branch to the skin of the inner side of the thigh ; and (6) the anterior 




Fig. 125.— Branches of the Lumbar Plexus. (After Hirschfeld and Leveille.) 
1, lumbar part of sympathetic cord. 2 and 2', twelfth dorsal nerve (anterior division). 
3, first lumbar nerve. 4, 4', ilio-hypogastric. 5, 5', ilio-inguinal. 6, second lumbar 
nerve. 7, 7', genito-crural nerve. 8, 8', external cutaneous nerve of thigh. 9, third lum- 
bar nerve. 10, fourth, n, fifth. 12, lumbo-sacral cord. 13, iliac branch of ilio-hypo- 
gastric. 14, its abdominal branch. 15, ilio-inguinal nerve. 16-17', external cutaneous 
nerve. 18, 18', genital branch of genito-crural. 19, 19', its crural branch. 20, anterior 
crural nerve. 21, 21', obturator nerve. 22, left sacral plexus. 23, aortic plexus of the 
sympathetic. 

crural (five millimetres in width), giving muscular branches to the 
anterior periphery of the thigh and having also cutaneous branches 
— middle cutaneous, internal cutaneous, and the long or internal 
saphenus nerve (cf. Figs. 123 to 126). 

All the nerves of this plexus contain sensory as well as 
motor fibres, and may hence be affected in both ways. How- 



LESIONS OF THE LUMBAR NERVES. 



367 



dependency, where- 



ever, these affections do not often appear 
as they are frequently ob- 
served as symptoms of cen- 
tral, more especially of spinal 
diseases, and, above all, of 
tabes. Our description of 
them, therefore, will here be 
very brief. 

Among the sensory dis- 
turbances we have first to 
mention the lumbo-abdominal 
neuralgia, in which the hip 
joint is affected in much the 
same way as the shoulder 
joint in cervico-brachial neu- 
ralgia, so that the whole lum- 
bar region down to the but- 
tock is intensely painful. Of 
greater practical importance 
is what Cooper has described 
as " irritable testicle," neu- 
ralgia spermatica or neuralgia 
of the testicle, which either 
only forms a part of the lum- 
bo-abdominal neuralgia, or, 
as Eulenberg and others as- 
sume, is a neuralgia of the 
sympathetic nerve. The spon- 
taneous pain and the tender- Fig . I26 .-deep1<erves of "anterior akd 
ness may attain such a degree 
as to lead to states of tempo- 
rary psychical exaltation. 
Generally only one testicle is 
affected and most of the in- 
stances are found in young 
people. Further, we would 
mention the crural neuralgia 
and the obturator neuralgia, 
affections which manifest 
themselves by pain following 
exactly the course of the respective nerves. The existence of 
tender points is not constant and their seat varies. 




Inner Part of the Thigh. (After 
Hirschfeld and Leveille.) 1, anterior 
crural nerve. 2-3, muscular branches. 4, 
internal and middle cutaneous nerves, di- 
vided to show the deeper branches. 5, 6, 
nerves to the pectineus. 7, cutaneous fila- 
ment from the last. 8, inner branch of in- 
ternal cutaneous nerve. 9-1 1, muscular 
branches. 1*14, internal saphenous nerve 
and its branches. 15-19, obturator nerve 
and its branches. 20, lumbo-sacral cord. 
21, its union with the first sacral nerve. 22, 
lumbar and sacral part of the sympathetic 
nerve. 23, external cutaneous nerve. 



3 68 



DISEASES OF THE SPINAL NERVES. 



The treatment must be carried out according to the princi- 
ples which we shall describe later in our account of sciatica. 

Even less frequently than the sensory do the motor disturb- 
ances occur by themselves. If present, thej' are mostly of 
spinal, rarely of peripheral origin. Paralyses in the distribu- 
tion of the crural nerve, which interfere with the function of 
the ilio-psoas and the quadriceps, make it impossible for the 
patient to bend the thigh at the hip joint and to extend the leg 
after it has been flexed on the thigh. Paralyses of the obtura- 
tor nerve interfere with the adduction of the thigh, and the 
patient is no longer able to cross the affected leg over the 
other. Disorders in the nerves of the gluteus, the tensor vagi- 
nas femoris, and the pyriformis impair rotation of the thigh 
inward and outward. Abduction is also hindered, while the 
actions of walking, standing, and more especially climbing 
stairs, are performed awkwardly. For details the reader is 
referred to Duchenne-Wernicke, page 261 and following, where 
the normal and pathological physiology of these muscles is 
carefully discussed. 

IV. Diseases of the Sacral and Coccygeal Nerves. 

The posterior small branches of the sacral nerves, four of which 
leave the vertebral canal through the posterior sacral foramina and 
the fifth through the foramen between the sacrum and coccyx, form 
numerous anastomoses, and thus constitute what is known as the 
posterior sacral plexus. The anterior, much larger, branches pass 
into the pelvis, where the first three and a part of the fourth, to- 
gether with the lumbo-sacral cord (resulting from the junction of the 
fifth and a part of the fourth lumbar nerves), go to form the (ante- 
rior) sacral plexus. The plexus is triangular in form and rests upon 
the pyriformis muscle. The several nerves unite without much in- 
terlacement into an upper, large, and a lower, small, cord or band. 
The upper is formed by the union of the lumbo-sacral cord with the 
first and second and the greater part of the third sacral nerves and 
is continued into the great sciatic nerve. The lower becomes the 
pudic nerve. The plexus gives origin to a number of collateral 
branches — the superior and inferior gluteal, the small sciatic, and 
perforating cutaneous nerves and branches to the pyriformis, obtura- 
tor internus, gemelli, and quadratus femoris. The great sciatic nerve, 
the largest nerve of the body, divides into the internal popliteal and 
external popliteal or peroneal, the latter again dividing into the 
anterior tibial and musculo-cutaneous, the former, which becomes 
the posterior tibial, terminating in the internal and external plantar 



LESIONS OF THE SACRAL PLEXUS. 



369 



nerves. The pudic nerve divides into the inferior hemorrhoidal, the 
perineal nerve, and the dorsal nerve of the penis or clitoris. 

The anterior branch of the coccygeal nerve is distributed to the 
integument over the back part and the side of the coccyx. It is 
joined by a branch from the fifth sacral nerve, while the posterior 
division is lost in the fibrous structures on the back of the coccyx. 

The affections of the sacral plexus, which appear independ- 
ently of any other disease, are chiefly sensory in nature. Mo- 
tor disturbances, although they are perhaps numerically as 
common as the former, are in the great majority of instances 
symptomatic of spinal diseases. 

Sciatica. 

Among the sensory disturbances there is especially one 
disease which, owing to its relative frequency and obstinate 
resistance to treatment, has attained to much practical impor- 
tance — namely, the affection of the sensory fibres of the sciatic 
nerve, the sciatic neuralgia or sciatica, malum Cotunnii (Co- 
tugno, 1764). This may, as autopsies have shown, be due to 
an organic disease of the nerve, a genuine neuritis, or to a func- 
tional neurosis. In the former there exist varicose dilatations 
of the blood-vessels of the nerve, swelling, increase in volume, 
alterations in consistency, and a collection of serous exudation 
in the nerve sheath (Cotugno, Jasset). In the latter no anatom- 
ical changes can be detected. The neuritis may be due to dis- 
ease of the neighboring structures, to a tenosynovitis in the 
lower leg (Erb), to affections of the vertebras (spondylitis, car- 
cinoma), or may appear independently, in which case, leaving 
cold out of consideration for a moment, we have usually to 
deal with mechanical injuries, either as the consequence of 
wounds, fractures, or as the result of protracted pressure (tu- 
mors of the pelvis, aneurisms, hernia, uterus gravidus, engorge- 
ment of the venous plexus of the pelvis, habitual constipation, 
etc.). The occupation must, moreover, be taken into consid- 
eration in the aetiology of sciatica. It may exert an injurious 
influence in one of two ways, either through the overexertion 
which it entails or through the exposure to frequent sudden 
changes of temperature. Of the former we have instances in 
those who work with the sewing machine for weeks and 
months for several hours a day and in those who are always 
lifting heavy weights (stevedores, blacksmiths, etc.). To this 
24 



37Q 



DISEASES OF THE SPINAL NERVES, 



class is thought to belong- " le lumbago des forgerons" de- 
scribed by Maisonneuve (Hirt, Krankheiten der Arbeiter, iv, 
90). Of the latter we have instances in puddlers and those 
who work at smelting furnaces, etc. Sciatica is frequently 
seen among such people, and seems to affect more commonly 
the left leg, probably because in throwing the coal into the 
furnace it has to be extended more forcibly (Chiene, of Edin- 
burgh, and Hirt). 

As a symptom sciatica is often seen in spinal affections 
(myelitis, spinal meningitis), in diseases of the general nervous 
system, especially in tabes, where it often appears bilaterally, 
also in diabetes. As a sequela it has been described as follow- 
ing typhoid fever. Whether malarial intoxication can ever be 
the cause of it is uncertain. It is sometimes seen in the course 
of syphilis. In lead and mercury poisoning it plays an entirely 
secondary role. 

Symptoms. — Among the symptoms of sciatica pain is the 
most important. The motor disturbances which sometimes 
occur in the course of the disease — tremor, clonic spasmodic 
movements, the difficulty and awkwardness in moving which 
interfere to a greater or less extent with standing and walking 
— have to be looked upon simply as the result of the pain. 
This varies greatly. At first it may be dull and quite bearable, 
but later boring in character, extending over the whole lower 
extremity and persisting without intermission, so that it con- 
stantly occupies the attention of the patient and forces him to 
a frequent change of position ; or, again, it may appear in at- 
tacks, with intervals of comparative ease, so that the patient 
feels fairly comfortable and is able to follow his occupation. 
During the seizures it may be of such excruciating intensity 
that it can only be compared with Fothergill's faceache or the 
lancinating pains of tabes. 

The patient suffers usually more intensely at night after 
going to bed, or at least he complains more at that time, often 
because he can not bear the extension of the leg, often perhaps 
because his attention is then less liable to be distracted. Yet 
even in the daytime the pain may reach a considerable pitch, 
especially when the patient has been making attempts to walk 
or has been standing too much. He may have perfect ease for 
hours when lying quietly, and yet a few movements of flexion 
and extension of the affected extremity are sufficient to throw 
him back into the most distressing condition. The extent of the 



LESIONS OF THE SACRAL PLEXUS. 



371 



pain also varies ; generally it is felt over the whole posterior 
surface of the thigh and the distribution of the external poplit- 
eal nerve. It may radiate into the region of the healthy sciatic 
and the lumbar plexus of the affected side. The posterior 
tibial nerve usually remains intact. Examination almost always 
discloses the existence of tender points, one, for instance, at 
the exit of the nerve from the pelvis, one at the lower margin 
of the gluteus, one in the popliteal space, one on the capitulum 
fibulas. There may be others, but their occurrence is uncer- 
tain and their position changeable. 

Sometimes patients with sciatica are seen to put all their 
weight upon the healthy leg in order to diminish the pain in 
the affected extremity. This causes the trunk to be bent to- 
ward the healthy side and the costal margin to approach the 
ilium, a position which may become so habitual that a genuine 
scoliosis may be developed (Albert, Nicoladoni, Babinski, cf. 
lit.). I have known several cases in which this secondary 
scoliosis persisted after considerable improvement of the pri- 
mary affection, whereas in other instances I have seen it dis- 
appear when the cure of the sciatica was complete. 

If we have to deal with a genuine neuritis trophic changes 
will be found to develop, especially more or less marked atro- 
phy of the muscles, with reaction of degeneration (Nonne). 
The patellar reflex seems in such cases to be considerably di- 
minished. An exaggerated knee jerk in the course of a periph- 
eral' neuritis has, on the whole, to be looked upon as excep- 
tional (Striimpell, Mobius). In sciatica I have never seen it. 
If the trouble is purely functional the muscles and reflexes re- 
main, even after years of suffering, unaltered. Other sensory 
changes — diminution of the sensibility, anaesthesias, paresthe- 
sias^ — occur, but take a very secondary position to the domi- 
nating feature of the disease, which is pain. 

Course. — The course as well as the duration vary greatly, 
but we may state as an undeniable fact that it is exceptional 
to find cases which last but a short time and end with com- 
plete recovery. Mostly it is a question of months and years 
before any decided lasting improvement is brought about. 
On the other hand, remissions are not rare. They may last 
for months and the condition of the patient may be such that 
he begins to be confident of a permanent cure, when suddenly, 
often without any appreciable cause, sometimes in consequence 
of a long walk, the pain again makes its appearance with un- 



oy2 DISEASES OF THE SPINAL NERVES. 

diminished intensity and the treatment has to be started all 
over again. The more frequent such relapses, the more gloomy 
becomes the outlook for complete recovery. 

Diagnosis. — Great care should be exercised in the diagno- 
sis, and we should first endeavor to decide whether the trouble 
has to be regarded as an idiopathic affection or as a symptom 
of another malady, and more especially in bilateral sciatica 
should we be on the lookout for a spinal disease or a disease of 
the general nervous system, such as tabes. The examination 
of the urine for sugar should never be omitted. If this proves 
negative, and if we can exclude general nervous diseases with 
certainty, we should proceed to analyze the pain, to examine 
into its nature, the time of its occurrence, its seat and extent, 
and should keep in mind that there are other than nervous af- 
fections that are associated with violent pain in the lower ex- 
tremities, for instance, acute rheumatism of the lumbar muscles, 
lumbago, also inflammations in the hip joint, chronic hip dis- 
ease, malum coxas senile, as well as gouty affections and psoas 
abscesses. In all such instances the immobility of the extrem- 
ity, which also exists in a pure sciatica, makes the examination 
difficult, and only after persistent repetitions shall we be able 
to obtain a clear idea as to the true nature of the trouble. Al- 
though it may be going too far to say with Hutchinson that 
out of twenty cases diagnosticated as sciatica in nineteen there 
exists no trouble whatever in the nerve (Medical Times and 
Gazette, 1882, vol. i, No. 1648, page 35), there can be no ques- 
tion but that here many diagnostic sins are committed and 
that there are many cases called sciatica after a superficial ex- 
ploration which later prove to be something entirely different. 

Treatment. — The treatment of sciatica should vary accord- 
ing as the neuralgic pains constitute merely a symptom or re- 
sult from an independent affection of the nerve itself. In the 
former case our therapeutic measures, of course, must be di- 
rected against the underlying disease (diabetes, tabes, syphilis, 
etc.). If we have to deal with sciatica as an affection by it- 
self our treatment should be systematic and carried out on 
definite lines. Our first rule should be never, or at any rate 
only in exceptional instances, to withdraw blood. If there are 
old scybalous masses in the bowel which press upon the nerve 
and thus cause the pain, considerable and lasting improvement 
may be brought about by the removal of these, and a course 
at Carlsbad or Marienbad may cure sciatica in such cases 



LESIONS OF THE SACRAL PLEXUS. 373 

more quickly and surely than the most careful use of electrici- 
ty. Next, especially when we have grounds for suspecting 
an inflammatory condition of the nerve, we should trj^ the ap- 
plication of counter-irritants to the skin, fly-blisters or the so- 
called points de feu (with Paquelin's thermo-cautery). The 
former more particularly, which have been used by Cotugno 
and Valleix, deserve to be recommended, as they prove gen- 
erally very effectual if used early in the disease ; they may be 
applied along the course of the nerve on the thigh or in the 
sacral region (Anstie). Less benefit is usually derived from 
irritating inunctions and plasters, which may, however, be 
given a trial ; for instance, we may employ one of Betz's plas- 
ters — empl. oxycroc, 15.0 (^ss.); arg. nitr. pulv., 1.0 (grs. xv) — 
allowing it to remain on the skin until it drops off of its own 
accord. Among other drugs for inunctions besides veratrine 
[0.1 : 10 lard] the narcotics (preparations of opium, belladonna, 
hyoscyamus) may be useful. Finally, the chloride-of methyl 
spray may be recommended. This, however, should be used 
with great care ; otherwise it may be followed by a cellulitis, 
erysipelas, or even gangrene. The desired effect does not al- 
ways follow. 

From internal medicines I have never seen any lasting good 
results ; besides antipyrine and antifebrine, iodide of potassium 
has been used from time immemorial, also quinine and all the 
nervines. Recently solanine has been recommended, fifteen to 
twenty centigrammes (grs. ijss.-iijss.) a day. In my own expe- 
rience this drug does not possess much value ; neither does the 
oil of turpentine given internally in capsules containing fifteen 
minims ten or twelve times a day. In short, I consider all in- 
ternal medicines, unless the case be one of syphilis, as useless 
and inadvisable, for, owing to the long duration of the trouble, 
they would have to be taken for months with great detriment 
to the stomach and to the digestion. More is accomplished 
by external measures — massage and electricity. Both have the 
disadvantage, however, that they act verv slowly and that their 
application causes more or less violent pain, a remark which 
applies more particularly to a systematic and an energetic use 
of massage (Schreiber and others). The faradic brush and the 
combined current used by De Watteville are also very painful, 
but both can be recommended with a clear conscience. With 
regard to the best manner in which the electricity should be 
given, as we have already said before we now repeat that every 



374 DISEASES OF THE SPINAL NERVES. 

one has his own method, in which he has most confidence be- 
cause he is most familiar with it. 

If we are forced to send our patients to the springs, we may 
first of all recommend non-medicated hot springs or hot brine 
springs. Among the former may be mentioned Gastein, Johan- 
nisbad, Teplitz-Schonau, and Wildbad ; among the latter, Wies- 
baden, Nauheim, Rehme, and Baden-Baden. At hot sulphur 
springs, for instance, Landeck, Teplitz-Trencsin, and Pistyan in 
Hungary, such patients do very well, but it is advisable not to 
raise their expectations too high, as often the results of a stay 
at the springs are not very conspicuous. Sea-bathing is not 
always borne well by patients with neuralgia. At any rate, it 
is well to begin with places on the Baltic and to select first 
those where warm sea-water baths can, if necessary, be also 
obtained — e. g., Colberg, Misdroy, Zoppot, and others. In 
severe cases, particularly if there occur transient attacks of 
intense pain, morphine can not be dispensed with. Subcuta- 
neous injections in proper amounts and at the proper time 
will do the patient no harm, but will afford him unspeakable 
relief, such as can be expected from no other drug. 

Far less frequently — we might say, only exceptionally — are 
the individual branches of the sciatic nerve the seat of neural- 
gia ; thus we may have an affection of the plantar nerves, and 
sometimes the hyperesthesia in their distribution may be so 
marked that the patient is absolutely prevented from standing 
or walking. Barbillon (cf. lit.) has devoted a careful study to 
this so-called plantar hyperesthesia without, however, being 
able to decide whether the disorder is of spinal origin, or 
whether it has to be regarded as a so-called dermatalgia, or 
again as a disturbance in the nutrition of the fine nerve end- 
ings. The first explanation is supported by the fact that 
usually both feet are affected ; the last that it often occurs in 
people who have to stand a good deal. It has often been 
known to occur as a sequela of typhoid fever. Cures are said 
to have been effected by blisters, or by the application of a 
spray of methyl chloride ; bathing the feet for some time in 
hot salt solution has also been recommended. 

The pudic nerve, which supplies the bladder, the rectum, 
the perinasum, and the external genitals, is often the seat of neu- 
ralgias which are sometimes purely cutaneous and show them- 
selves by an extreme tenderness of the skin of the penis, the 



LESIONS OF THE SACRAL PLEXUS. 



375 



scrotum, the region of the anus, and the mons Veneris. In 
many instances the testicle is affected and, as we have pointed 
out above, becomes very tender and the seat of violent paroxys- 
mal pains. Although there may be intervals in which the neu- 
ralgia disappears, the tenderness and irritability remain as long 
as the disease of the nerves is present. 

Other nervous affections of the male urinary apparatus have 
been studied by Oberlander (cf. lit.), who has called attention 
to the fact that varicocele, chronic gonorrhoea, hydrocele mul- 
tilocularis, tuberculosis, carcinoma, etc., frequently give rise to 
such disorders, and indeed not only do the just-mentioned cuta- 
neous forms occur, but also a peculiar neuralgia of the urethra, 
which becomes particularly distressing during coitus and mic- 
turition, is frequently known to develop under the influence of 
such affections. The remains of a gonorrhoea together with 
chronic dyspepsia may produce a chronic hyperaesthesia of the 
mucous membrane of the bladder, to which little attention has 
been paid as yet. The pain appears periodically, affects the 
whole bladder region, and radiates into the urethra and the 
ureters. Slight errors of diet may evoke violent exacerbations 
of the trouble. Neuralgia of the bladder is found in neurasthe- 
nia, but also at times in the initial stage of tabes ; hence it would 
be necessary to decide, if we have diagnosticated a neuralgia of 
the bladder, whether it is due to a cystitis or a spinal disease, 
or whether, on the other hand, it constitutes an affection by itself. 

Anaesthesia of the mucous membrane of the bladder and of 
the urethra as well as loss of the muscular sense of the bladder 
make it impossible for the patient to say with the eyes closed 
whether he is voiding urine or not. It may happen to tabetics, 
in whom the condition is not infrequently met with, that, hav- 
ing given up all attempts to micturate after unsuccessful strain- 
ing, they pass their urine involuntarily and become only con- 
scious of the fact when they feel the dampness of their clothes. 
This anaesthesia does not seem, however, to occur as an inde- 
pendent disease, but would appear to be always of central 
origin. 

The motor disturbances affecting the muscles which expel 
the urine and those which close the bladder may be of an irri- 
tative or a paralytic nature, the former constituting what is 
known as strangury ; the latter are by the laity comprehended 
under the name of " weakness of the bladder." Both may be 
symptoms of chronic inflammation of the urethra or of certain 



376 DISEASES OF THE SPINAL NERVES. 

spinal diseases, and may also occur independently, as purely 
nervous affections. The desire to urinate every few minutes, 
a desire which is increased after drinking alcoholic beverages, 
is not infrequently alternated by spastic conditions of the mus- 
cles of the bulb which give rise during micturition to spas- 
modic excruciating pains in the perinaeum which radiate to the 
thighs and the buttocks. 

In all cases of this kind the treatment is generally begun with 
the usual anti-neuralgic remedies, of late years also with co- 
caine. However, the result is often very unsatisfactory. We 
should always carefully search for possible underlying abnor- 
mities, such as an elongated adherent preputium, insufficiently 
dilated or tight strictures, flexion or version of the uterus, or 
pathological changes in the rectum. If such be found the neu- 
ralgia is to be regarded as a reflex neurosis and we have to di- 
rect our therapeutic efforts to the primary cause, by which 
procedure we may be able to improve and eventually cure the 
neuralgia. To the same class of reflex neuroses belongs the 
enuresis nocturna, which is rather common among children. 
The trouble can usually be traced to irritation in the urethra 
or at the orifice, such as inflammatory conditions, slight adhe- 
sions of the mucous membrane far back in the urethra, too nar- 
row an orifice of the urethra, and the like. Here, of course, 
attention to such primary disorders is the first step in our 
treatment, and dilatation of the posterior portions of the ure- 
thra with dilators made for the purpose will often be followed 
by striking results (Oberlander, Berliner klinische Wochen- 
schrift, 1888, 31). 

By coccygodinia we mean a neuralgia which is character- 
ized by pain over the region of the coccyx. The affection is 
more frequently met with in women than in men, and the pain, 
which shows paroxysmal exacerbations and comes on more par- 
ticularly during the act of defecation, may attain to a frightful 
pitch. The causes of the affection are obscure, yet we are 
probably not far from being correct in assuming that in many 
cases it is of reflex origin, as in men especially treatment of the 
genitals — a diminution of an abnormal sensitiveness of the pars 
prostatica ureth., etc. — may be followed by surprising results. 
In some cases the pains appear during sleep without any ap- 
preciable cause, in others they have been known to occur after 
traumatism. I have repeatedly observed them in neurasthenics 
and hysterical patients. The excision of the coccyx, an opera- 



LESIONS OF THE SACRAL PLEXUS. 



177 



tion which in desperate cases has been undertaken for relief of 
the pain, should, of course, not be resorted to until all other 
means, particularly energetic application of the faradic brush, 
have been thoroughly tried. 

LITERATURE. 

Hammond. Neuralgia of the Testicle. Neurolog. Contribut, 1881, i, 3. 

Sutton. Crural Neuralgia in Dentists. Lancet, 1882, ii, 4. 

Engelhardt. Zur Genese der nervosen Symptomencomplexe bei anatomischen 

Veranderungen in den Sexualorganen. Stuttgart, Enke. 
Englisch. Ueber eine besondere Form der Hamorrhagie an den Unterextremi- 

taten (Haemorrhagica neuralgica). Wien. med. Blatter, 1885, 24-26. 
Barbillon. On Hyperesthesia plantae bilateralis. Progr. med., 1885, xiii, 19. 
Striimpell und Mobius. Ueber Steigerung der Sehnenreflexe bei Erkrankung 

peripherer Nerven. Munch, med. Wochenschr., 1886, xxxiii, 14. 
S. Laache. Norsk Magaz. f. Lagevidensk., 1886, 4 R., i, 19. (Hyperesth. 

plantar.) 
Oberlanuer. Zur Kenntniss der nervosen Erkrankungen am Harnapparate des 

Mannes. Volkmann'sche Sammlung klin. Vortr., 1886, 275. 
Adamkiewicz. Ein seltener Fall von Neuralgie im N. pudendus communis mit 

gliicklichem Ausgange. Bresl. arztl. Zeitschr., 1886, 8. 
Potherat. Neuralgie vesicale. Progres med., 1887, 27. 
Nonne. Berl. klin. Wochenschr., 1887, 45. 

Hughes (St. Louis). Weekly Med. Rev., March 12, 1887. (Plantar hyperes- 
thesia, neuritis N. plantaris interni, in consequence of overexertion). 
Peyer. Zwei Falle von Neuralgie des Steissbeins bei Mannern. Centralbl. f. 

klin. Med., 1888, ix, 37. 
Bernhardt. Klin. Beitrag zur Lehre von der Innervation der Blase des Mast- 

darms und der Geschlechtsfunction. Berl. klin. Wochenschr., 1888, xxv, 

32. 
v. Swiecicki. Zur operativen Behandlung der Coccygodynie. Wien. med. 

Presse, 1888, xxix, 31. 
Grafe, M. Zeitschr. f. Geburtsh. und Gynacologie, 1888, xv, 2, p. 344. 

As to the motor disturbances — and of these we will take up 
first the paralyses which occur in the distribution of the sacral 
plexus — here, too, those of the sciatic nerve are the most im- 
portant. Such lesions may affect the nerve high up in the 
pelvis, or soon after its exit from it, or still lower down in its 
branches. The first are almost always caused b}^ traumatism 
or pressure exerted for a comparatively long time — e. g., by a 
pregnant uterus, the child's head during labor (Vinay), tumors, 
etc. The others often constitute a symptom of some other 
disease. 

External popliteal (peroneal) paralysis, in which the mus- 
cles of the anterior surface of the leg are affected (the extensors 



37* 



DISEASES OF THE SPINAL NERVES. 



of the toes, the tibialis anticus, and the peronei), is easily rec- 
ognized. The foot hangs down flaccidly, it can neither be 





Fig:. 127- Fig. 128. 

Fig. 127.— Cutaneous Nerves of the Leg and Foot. (After Hirschfeld and 
Leveille.) 1 and 2, external popliteal nerve and its cutaneous branch. 3, peroneal 
communicating branch which unites with 4, the tibial communicating, in 5, the external 
saphenous nerve. 6, calcaneal branch of the external saphenous nerve. 7, external dor- 
sal digital branch to the fifth toe. 8, dorsal digital branch to the fourth and fifth toes. 
9-12, musculo-cutaneous nerve. 13, anterior tibial nerve. 14, its inner terminal branch 
between the first and second toes. 15, recurrent articular nerve. 

Fig. 128. — Distribution of the Branches of the External Popliteal Nerve. 
(After Hirschfeld and Leveille.) a, tibialis anticus muscle. 6, long extensor of 
great toe. c, peroneus longus. 1 and 1', external popliteal nerve. 2 and 2', musculo- 
cutaneous nerve. 3, 3', internal branch of musculo-cutaneous nerve. 4, its external 
branch. 5, external saphenous nerve. _ 5', its branch to outer side of fifth toe. 6, 6', 
6"-8, anterior tibial nerve. 

dorsally flexed, abducted, nor adducted. As a result of this, 
walking is very much impaired, since the point of the foot 



LESIONS OF THE SACRAL PLEXUS. 



379 



often trips over prominences on the floor, but by raising the 
thigh higher than usual the patient somewhat overcomes the 
difficulty. As the point of the foot or the outer margin is first 
put to the ground in an awkward manner, the gait is very 
peculiar and highly characteristic of this form of paralysis. 
Contractures of the calf muscles, which may later develop sec- 

..■■' M _, N. cruralis 



N. obturator 
M. pectineus 

21. adductor magnus 
M. adductor longus 



M. tensor vagina; 
fcmoris 



M. quadriceps fcmoris 
rectus femoris 
crurcus 

M. vastus ezternus 

M. vastus intcrnus 

M. gastrocnemius 
\ solcus 



M. flexor longus 
pollicis 

'. abductor minimi 
digiti 



M. interossci dorsal cs 



Fig. 129. — Motor Points for the Nerves and Muscles of the Anterior Sur- 
face of the Leg. 



N. poplilecdis ezternus 
M. tibialis anticus 
M. extensor longus 
digitorum 

M. peroneus lorigus 
M. peroneus brevis 

M. extensor brevis 
pollicis 



extensor brevis 
diqitorum 




ondarily, give rise to a permanent position of talipes equinus 
or talipes equino-varus. External popliteal paralysis may be 
brought on by the occupation of the patient. It has been seen 
as the result of pressure in those who, from the nature of their 
work, have to be constantly in a kneeling position, as, for in- 
stance, asphalt pavers (Bernhardt). 



38o 



DISEASES OF THE SPINAL NERVES. 



Internal popliteal paralysis, which concerns the muscles of 
the back of the lower leg (the flexors, the tibialis posticus) and 
the muscles of the soles of the foot (adductor and abductor 
hallucis and the interossei), interferes with the plantar flexion 
of the foot and with flexion and lateral motion of the toes. As 
a result the patients are unable to stand on tiptoe. If the in- 
terossei take part, a condition is developed similar to that 



Biceps femoris 
(long head) 



Biceps femoris 
(short head) 



External popliteal 
nerve 




Gluteus maximus 

Sciatic nerve 
Adductor magnus 
Semitendinosus 
Semimembranosus 



Internal popliteal 

nerve 



Gastrocnemius 
(external head) 

Gastrocnemius 
(internal head) 

Solcui 



Flexor communis 

digitorum 
M. flexor longus pollicis 

Posterior tibial nerve 



Fig. 130. — Motor Points for the Sciatic Nerve and the Muscles supplied by 



which is seen in the hand and which we have described on 
page 348. The toes assume a claw-like position owing to the 
fact that the first phalanx is dorsally flexed while the second 
and third are in plantar flexion. Here also secondary con- 
tractures may appear (of the tibialis anticus, triceps suras), 
which give rise to a paralytic clubfoot (pes planus, pes equinus, 
pes calcaneus). 

Paralysis of the whole sciatic, which also, as we know, sup- 
plies the flexors of the lower leg (the semitendinosus, the semi- 



LESIONS OF THE SACRAL PLEXUS. 



381 



membranosus, and biceps femoris), makes it impossible for the 
patient to flex the lower leg on the thigh, to approach the 
heel to the buttock, and to rotate the thigh (M. obturator in- 
ternus). Paralysis of one sciatic alone does not make walking 
absolutely impossible, because the leg fixed in the knee joint is 




Fig- I3 1 -— Case of Peripheral Neuritis of the Sciatic Nerve with Shortening 
and Atrophy of the Affected Extremity (personal observation). 

moved forward by the muscles of the thigh, and so is used as a 
stilt (cf. page 228, gait of the hemiplegic). After a certain time 
muscular atrophies begin to be noticeable, and later become 
very marked. The affection of the hip joint, which sometimes 
develops in the course of the paralysis, but which also at times 
has to be looked upon as the forerunner or immediate cause of 
the paralysis, produces more or less marked shortening, so that 
the patient with his affected lower extremity presents a picture 



382 



DISEASES OF THE SPINAL NERVES. 



like one of those shown in Figs. 131 and 132. This peripheral 
affection of the sciatic, which has to be regarded as a neuritis 
in the sense described above on page 328, can hardly be mis- 
taken for anything else. The difficulty in moving one leg, 
which may amount to an actual paralysis, may, it is true, also 



» 



/* 




Fi S- 132.— Case of Peripheral. Neuritis of the Sciatic Nerve with Shortening 
and Atrophy of the Affected Extremity (personal observation). 

be the consequence of a central cortical affection — a mono- 
plegia or monoparesis. In this case, however, the pains are 
by no means a prominent symptom, nor do we find — and this 
is the most important point of distinction — either atrophy or 
shortening. The differential diagnosis between cortical and 
peripheral paralysis has been spoken of on page 183. The 
treatment of the affection is to be conducted according to the 
principles which we have discussed in speaking of other periph- 
eral paralyses. 



LESION'S OF THE SACRAL PLEXUS. 



333 



The observations which some years ago were published by West- 
phal about a periodically recurring paralysis of all four extremities 
have as yet no practical importance, since we do not know anything 
about its nature. The same may be said about the peculiar paresis 
of the lower leg and foot which Zenker has described (Berliner klin- 




Fig. 133- 
Figs. 133-134. — Contracture 



Fig. 134- 
CHE Quadratus LuMBORUM (personal observation). 



ischer Wochenschrift, October 8, 1883), and which has to be regarded 
as an occupation neurosis. It occurs not rarely in persons who have 
to remain a long time in a kneeling or squatting position, and such 
instances have been known to occur in potato pickers. It manifests 
itself in a more or less pronounced sensory or motor paralysis of the 
lower part of one or both lower extremities. 

Spasms of the nerves of the sacral plexus may be tonic or 
clonic in character. They are, however, rare, and since treat- 



3§4 



DISEASES OF THE SPINAL NERVES. 



ment can do but little against them they are not of much prac- 
tical interest. 

Spasmodic tonic contraction of the hip muscles has been 
described by Stromeyer as spastic contraction of the hip. A 
case of spasm confined to the quadratus lumborum has come 
under my notice in an hysterical woman. It is illustrated in 
Figs. 133 and 134. Tonic spasm of the quadriceps gives rise to 
extension of the leg in the knee joint ; it is sometimes known 
to occur in neuralgias of the joint. The very painful cramp in 
the calf muscles, which sometimes occurs after great exertion, 
sometimes also in the course of certain grave general diseases 
— for example, cholera — is well known. 

Clonic spasms of the muscles of the lower extremities may 
be observed in hysterical patients. The so-called " saltatory 
spasm " (Bamberger, Wiener medicinische Wochenschrift, May 
4, 1859), which forces the patients whenever their feet touch 
the ground to jump, is not an independent affection, but only a 
symptom of central disease. The increase of the reflexes, 
which is generally present, is in favor of this view. Of the 
treatment we shall speak in the chapter on hysteria. 

LITERATURE. 

Albert. Eine eigenthiimliche Art der Totalscoliose. Wien. med. Presse, March 

1, 1886, xxvi. 
Nicoladoni. Ueber eine Art des Zusammenhanges zwischen Ischias und Scoli- 

ose. Ibid., 1886, 26, 27. 
Vinay. Paralysie radiculaire du nerf sciatique par compression a cause de 1'ac- 

couchement. Revue de med., 1887, 7. 
Babinski. Sur une deformation particuliere du tronc causee par la sciatique. 

Arch, de neur., 1888, xv, 43, 1. 
Bernhardt. Ueber Peroneuslahmungen. Original-Bericht der Gesellsch. f. 

Psych, u. Nervenkrankheiten zu Berlin am 12. Nov. 1888. Neurol. Cen- 

tralbl, 1888, 23. 
Schiidel. Ueber Ischias scoliotica. Arch. f. klin. Chirurgie, 1888, 38, 1. 
Weiss. Zur Therapie der Ischias. Centralbl. f. d. gesammte Therapie, 1889, 

vii, 1. 
Guttmantn. Fall von sogenannten saltatoiischen Krampfen. Berl. klin. Woch- 

enschr., 1867, iv, 13. 
Frey. Ueber saltatorischen Reflexkrampf. Arch. f. Psych, u. Nervenkh., 1875, 

vi, 1. 
Kast. Ueber saltatorischen Reflexkrampf. Neurol. Centralbl., 1883, ii, 14. 
Kollmann. Deutsche med. WochenscHr., 1883, ix, 40. 



MULTIPLE NEURITIS. 



385 



V. Neuritis involving Several Spinal Nerves at the Same Time — 
Multiple Neuritis — Polyneuritis. 

Just as we have seen that several of the cranial nerves can 
be affected at the same time, so none the less is this true of the 
spinal nerves. It is, however, not many years since it has been 
shown that such multiple nerve affections may occur primarily, 
that they are often of an inflammatory nature, that they give 
rise to numerous symptoms which may, under certain circum- 
stances, be misinterpreted, inasmuch as they may simulate 
those of central lesions. The affection is known as multiple 
neuritis, and, as we said, our knowledge of it is of quite recent 
date (Dumenil, Eisenlohr, Leyden, Striimpell, Vierordt, and 
others). We may confidently expect that in the near future we 
shall obtain further information upon certain points in connec- 
tion with this disease which have not as yet been cleared up. 

As .we have above, on page 328, devoted some time to the 
description of the anatomical features of the disease, it remains 
for us here to speak first of the symptoms of multiple neuritis. 
It is remarkable to note that the onset frequently resembles 
that of an acute infectious disease : there is fever, general 
malaise, dull headache, apathy, etc. ; soon pains make their 
appearance, first in the lumbar region and the back, then in 
the course of the large nerve trunks. These are followed by 
an impairment of mobility, especially in the lower extremities, 
which makes the patient very anxious ; the legs are heavy, 
they are moved only by a strong effort, and not without pain, 
and the patient is easily fatigued. The reflexes are diminished 
or lost, electrical excitability is decreased, but the pains — and 
this should be emphasized — usually soon abate and other sen- 
sory disturbances, parassthesias and anaesthesias, are only 
exceptionally met with, the disorder chiefly affecting the 
motor apparatus. Repeatedly cases have been observed in 
which the motor disturbances made their appearance quite 
suddenly, an onset which we could almost call apoplectiform. 
Without any premonitory symptoms there come on violent 
radiating pains, with motor paralysis and trophic changes. 
Muscular atrophy and reaction of degeneration can be de- 
monstrated. The muscular atrophy sometimes shows itself 
early and attains a high grade, sometimes not until late, and 
may be so slight that it almost escapes notice. In many in- 
25 



3 86 



DISEASES OF THE SPINAL NERVES. 



stances a certain amount of ataxia is observed, and this symp- 
tom may indeed be very marked, so that it dominates the 
whole picture and makes it resemble that of tabes. In such 
cases the term pseudo-tabes peripherica, instead of simply 
multiple neuritis or polyneuritis, is very appropriate. 

No description of the course of the disease which would 
fit all cases is possible, because this varies and presents pecul- 
iarities according to the pathogenesis. For example, if a mul- 
tiple neuritis occurs in the course of another disease, its mani- 
festations are not the same as when it is a primary affection, 
which has developed under the influence of some special cause. 
Among the conditions in which polyneuritis may develop we 
would mention phthisis pulmonalis, diabetes, tabes, articular 
and muscular rheumatism, polyarthritis, and finally the puer- 
peral state. It has repeatedly been described as a sequela of 
typhoid fever, of small-pox, scarlet fever, and of diphtheria (the 
" infectious form " of Leyden). As an independent disease it 
may be caused by overexertion. Two cases which we have 
described were due to prolonged work with the sewing ma- 
chine (cf. lit.). It may also appear, and this is unquestionably 
much more common, as a consequence of the action of cer- 
tain poisons, more especially alcohol, carbon monoxide, bisul- 
phide of carbon, lead, arsenic, and mercury (the "toxic form " 
of Leyden). Besides these two there is, according to Leyden, 
a third variety, the so-called atrophic (ansemic, cachectic) form, 
which develops after a long and severe sickness, somewhat in 
the manner recently described by Oppenheim and Siemerling. 

Sometimes sensory, sometimes motor disturbances are the 
predominating symptoms. In the neuritis of phthisical patients 
both are marked to about the same extent. Occasionally cer- 
tain nerves seem to be more liable to suffer — for instance, ac- 
cording to Mobius, during the puerperal state, the median and 
ulnar, the terminal branches of which are affected either in 
both hands or only in the one which is used more extensively, 
as a rule the right. In tabes, on the other hand, no region 
seems to be exempt, and, as Oppenheim, Siemerling, Pitres, 
Vaillard, and others have observed, not only the peripheral 
spinal, but also the cranial nerves may be attacked by the 
neuritis — for example, the vagus and its laryngeal branches, 
and the ocular nerves. 

The neuritis which occurs in the course of joint affections 
often leads to considerable atrophy in those muscles which are 



MULTIPLE NEURITIS. 



387 



supplied by the affected nerve twigs. Chronic inflammation of 
the synovial membranes caused by sprains, chronic inflamma- 
tions of joints, articular rheumatism, frequent attacks of gout, 
fractures which give rise to some impediment in circulation — 
all these causes may bring about extensive muscular atrophies. 
References bearing on these affections and upon " reflex atro- 
phies," which we shall soon mention, will be found on page 
393. The case which we have illustrated in Figs. 135 and 136 
was that of a young man who suffered from a panarthritis, and 
who in consequence of his joint affection developed muscular 
atrophy in all four extremities, more especially in the upper 
arms and thighs. The hip and shoulder joints, as well as the 
knee and elbow joints, had been swollen and painful for years. 
That this atrophy, which may be due to an inflammation of the 
fine end twigs of the nerves, may also be caused reflexly by 
the joint affection has been shown by Charcot. If the hip 
joint is attacked, the flattening of the buttock, the abnormally 
high position of the gluteal fold, the marked prominence of 
the trochanter on that side, are striking features. If the upper 
extremities, especially the hands, are the seat of the disturb- 
ance, the atrophy gives rise to deformities which are either of 
the extensor or the flexor type (Charcot). 

Peculiar and manifold are the manifestations of that variety 
of neuritis which is produced by the abuse of alcohol. For 
the sake of simplicity we may distinguish two cardinal forms 
of this affection, although the clinical pictures of the two can 
often not be well separated from each other. In the first the 
motor disturbances and the atrophies, in the second the sensory 
disorders, are the prominent symptoms. In the former case 
the patients complain of violent tearing and drawing pains in 
the lower, more rarely in the upper extremities, which are rela- 
tively rapidly followed by a marked difficulty in walking. The 
gait of the patient is distinctly ataxic and resembles most 
closely that of a tabetic, with the exception that in the latter 
no diminution in the strength of the muscles can be noted, 
while in alcoholic neuritis it can undoubtedly be demonstrated 
and is to be explained by the muscular atrophy which occurs 
comparatively early and which is particularly seen in the ex- 
tensors. The degree to which walking in particular and mo- 
tion in general is interfered with is very variable. Sometimes 
the patient can hardly raise himself in bed without assistance, 
sometimes he may for months be able to get about fairly well 



388 DISEASES OF THE SPINAL NERVES. 

without help. It is interesting to note that the patellar reflex 
is lost very early and completely, a circumstance which may 
lure not the inexperienced alone into making a diagnosis of 
tabes dorsalis. This is still more likely to occur, and the mis- 








Fig- 135- — Panarthritis with Secondary Multiple Neuritis. 

take^ is more excusable, if the action of the alcohol has also 
manifested itself on the ocular nerves, so that, e. g., we may, in 
addition to the symptoms mentioned, encounter a paralysis 
of the abducens, which I have myself seen several times in 
alcoholic neuritis, and which Suckling (cf. lit.) and others have 
described ; or, again, the oculo-motor may be implicated and the 
patient may complain of diplopia. Vagus neuroses have been 
reported in this connection, especially tachycardia, by Dejerine. 
If we add to this the frequency with which Romberg's sign 



MULTIPLE NEURITIS. 



389 



(swaying while standing with the heels and toes together and 
eyes closed, in consequence of the disturbance of the muscular 
sense) is found in the disease, if we remember that stomach 
symptoms occur in both affections — in alcoholism as vomitus 




Fig. 136.— Panarthritis with Secondary Multiple Neuritis. 

matutinus in consequence of a chronic gastritis, in tabes as gas- 
tric crises in consequence of disease of the vagus nucleus — we 
can not be surprised at the frequency with which alcoholic 
paralysis is taken for tabes. Nevertheless it is not so difficult 
to avoid such a mistake, more especially if we have a chance to 
examine the patient repeatedly and do it carefully enough. 
We should particularly note the condition of the pupils. The 
absence of the Argyll-Robertson sign and the absence of 
bladder symptoms, both of which are very common in tabes, 



390 



DISEASES OF THE SPINAL NERVES. 



will be significant features. In alcoholic neuritis, further, the 
nerve trunks are usually painful and the course of the dis- 
ease differs in the two maladies. In tabes, as we know, the 
outcome is very unfavorable, while in alcoholic neuritis, if the 
cause is removed, it is usually good. Even the individual 
symptoms may, if analyzed carefully, give us some valuable 
diagnostic hints. For example, it will hardly be very difficult 
for the careful examiner to distinguish the morning vomiting 
of alcoholics from the paroxysmal spontaneous vomiting of 
tabes, which appears now and again and may not reappear for 
months. 

The second form of alcoholic neuritis may run its course 
without giving rise to any decided motor disturbances. The 
patient then only complains of pains which sometimes run along 
the nerve trunks, becoming very violent, and may resemble the 
lancinating pains of tabes. He may complain of localized hy- 
peresthesias and anaesthesias, of formication and numbness, all 
of which symptoms are especially marked in the lower extremi- 
ties. Various vaso-motor and trophic disturbances are not un- 
common. CEdema may occur and disappear again, skin erup- 
tions, circumscribed areas of hyperidrosis, the falling out of 
the nails and hair, may be noted. In all cases the psychical 
condition ought not to be neglected. It may present changes 
very early in the disease. Thus Oppenheim has reported in- 
stances in which the alcoholic neuritis occurred simultaneously 
with delirium tremens. 

About the toxic form of neuritis, which is not uncommonly 
found as a consequence of the occupation, we shall speak in the 
chapter on intoxications. 

It has long been known that neuritis may be produced arti- 
ficially, and that it, for example, often occurs as a consequence 
of subcutaneous injections of ether ; but this has only been 
carefully studied of late years. Cases of this kind impress 
upon us the necessity of being cautious in giving the injections 
for therapeutic purposes and of avoiding especially a too deep 
insertion of the needle where we should be liable to strike 
branches of the musculo-spiral or other nerves. Paralysis of 
the extensors of the fingers has been relatively often observed. 
References bearing upon this subject will be found on page 
392 (cf. also page 345). 



MULTIPLE NEURITIS. 



391 



LITERATURE. 
a. Multiple Neuritis. 

Dejerine. Sur l'existence d'alterations des nerfs cutanes chez les ataxiques etc. 

Compt. rend, de la Soc. de Biol.. 1882, p. 215. 
The same. Note complementaire sur les alterations des nerfs cutanes dans 

l'Ataxie etc. Ibid., 1882, p. 215. 
The same. Sur le nervo-tabes peripherique (ataxie locomotrice par nevrites 

pe>iphe>iques) avec integrite absolue des racines posterieures, des ganglions 

spinaux et de la moelle epiniere. Gaz. de Paris, 1883, 44. 
Strumpell. Zur Kenntniss der multiplen degenerativen Neuritis. Arch. f. 

Psych, u. Nervenkrankheiten, 1883, xiv, 2. 
Hirt. Beitrag zur Pathologie der multiplen Neuritis. Neurol. Centralbl., 1 884, 2 1 . 
Leval-Piquechef. Des Pseudo-Tabes. These de Paris, 1885. 
Boeck. Tidsskr. f. prakt. Med., 1885, v, 18. 
Buzzard. On Some Forms of Paralysis dependent upon Peripheral Neuritis. 

November 28, December 12 and 19, 1885. 
Pitres und Vaillard. Arch, de Phys., 1885, v, ser. 3, p. 208. 
Oppenheim. Multiple Neuritis. Deutsch. Arch. f. klin. Med., 1885, Bd. 36, 

Heft 5, 6, p. 561. 
Buzzard. Paralysis dependent upon Peripher. Neuritis. Lancet, November 28, 

December 12, 1885. 
Pitres et Vaillard. Peripheral Neuritis in Tuberculosis. Rev. de med., 1886, 

No. 3. (Latent or associated with atrophy or sensory disturbances.) 
Francotte. Nevrite multiple. Revue de med., 1886, No. 5. 
Oppenheim. Ueber interstitielle Neuritis, ihr Vorkommen bei Nerven- und 

anderen Erkrankungen. Neurol. Centralbl, 1886, No. 11, p. 255 et seq. 
Massalongo. Le neuriti multiple periferiche primitive e specialmente della forma 

di polineurite acuta. Gaz. degli ospitali, 1886, Nos. 55, 56, 58-62. 
Pitres et Vaillard. Nevrites peripheriques dans le rhumatisme chronique. Re- 
vue de med., 1887, viii, 6, p. 456. 
Grimodie. Contribution a l'etude de la pathogenie des nevrites peripheriques. 

These de Paris, 1887. 
Rosenheim. Zur Kenntniss der acuten infectiosen multiplen Neuritis. Arch. f. 

Psych, u. Nervenkr., xviii, 3, 809. 
Mdbius. Ueber Neuritis puerperalis. Miinchener med. Wochenschr., 1887, No. 

9. (Attacks most frequently the ulnar and the median nerve.) 
Stadelmann. Neurol. Centralbl., 1887, 17. (Peculiar condition found in a case 

of neuritis of the brachial plexus coming on after typhoid.) 
Goldflam. On the so-called Multiple Neuritis. Medycyna, 1887, xv, 23 28. 
Eisenlohr. Berl. klin. Wochenschr., 1887, 42. 
Lallemand. Monographic des nevroses professionelles et leur traitement. These 

de Paris, April, 1887. 
Marie, P. La Paralysie de l'lsthme de Panama. Progr. med., 1887, xv, 9. (A 

kind of beri-beri.) 
Oppenheim und Siemerling. Beitrage zur Pathologie der Tabes dorsualis und 

der peripherischen Nervenerkrankungen. Arch. f. Psych, u. Nervenkr., 

1887, xviii, 1, 2. 



39 2 



DISEASES OF THE SPINAL NERVES. 



Dubois. Ueber apoplectiformes Einsetzen neuritischer Lahmungen. Corre- 

spondenzbl. f. Schweiz. Aerzte, 1888, 14. 
Senator. Ueber acute multiple Myositis bei Neuritis. Deutsche med. Woch- 

enschr., 1888, xiv, 23. 
Goldflam. Zeitschr. f. klin. Med., 1888, xiv, 4. 
Bury. Peripheral Neuritis in Acute Rheumatism and the Relation of Muscular 

Atrophy to Affections of the Joints. From the Medical Chronicle, June, 

1888. 

b. Alcoholic Neuritis. 

Fischer. Ueber eine eigenthiimliche Spinalerkrankung b. Trinkern. Arch. f. 

Psych., 1882. 
Dreschfeld. Brain, July, 1884, p. 200. (Chronic alcoholism : ataxia in men, 

atrophies in women.) 
Broadbent. On a Form of Alcoholic Spinal Paralysis. Med.-chir. Transact., 

vol. Ixvii. 
Charcot. Les paralysies alcooliques. Gaz. des hop., 1884, No. 99. 
Kruche. Die Pseudotabes der Alkoholiker. Deutsche Med.-Ztg., 1884, No. 

72. 
Moeli. Statist, u. Klin, iiber Alkoholismus. Charite-Annal., 1884, ix, p- 

524. 
Schulz. Neuritis der Potatoren. Neurol. Centralbl., 1885, Nos. 19, 20. 
Hadden. Cases Illustrating the Symptoms of Chronic Alcoholism. Lancet, 

October 3, 1885, p. 610. (Hyperassthesia of the skin, vomiting, no patellar 

reflex, plantar reflex retained.) 
Bernhardt. Ueber die multiple Neuritis der Alkohoolisten. Zeitschr. f. klin. 

Med., 1886, xi. 
Brissaud. Des paralysies toxiques. These d'agregation de Paris, 1886. 
Oettinger. Etude sur les paralysies alcooliques. These de Paris, 1885. 
Dejerine. Contribution a l'etude de la nevrite alcoolique. Arch, de Phys., 1887, 

x, 5me ser., p. 248. 
Witkowski. Zur Kenntniss der multiplen Alkoholneuritis. Arch. f. Psych, u. 

Nervenkrankheiten, 1887, xviii, 3, p. 809. 
Bonnet. Arch, de neurologic Juillet 1887, pp. 79 et seq. 
Suckling. Ophthalmoplegia externa due to Alcohol. Brit. Med. Journ., March 

3, 1888. 
Eichhorst. Neuritis fascians alcoholica. Virchow's Archiv, 1888, 112, 2. 
Siemerling. Kurze Bemerkungen zu der von Eichhorst sogenannten Neuritis 

fascians. Arch. f. Psych., 1888, xix, 3. 

c. Neuritis caused by Subcutan. Injection of Ether. 

Salvat. These inaug. Bordeaux, 1884. 

Remak und Mendel. Berl. klin. Wochenschr., 1885, xxii, 5, pp. 76, jy. 

Hadra. Sitzung der Berl. med. Gesellsch., v, 3. Juni 1885. 

Pitres et Vaillard. Des nevrites provoquees par les injections d'ether au voisi- 

nage des troncs nerveux des membres. Gaz. med. de Paris, 28* Mai 1887, 

No. 22. 



d. Musctclar Atrophy after Joint and Bone Disease—" Reflex Atrophy " 
(Charcot). 

Bonnet. Traite des maladies des articulations. Paris, 1845, i, p. 207. 

Roux, J. Ann. de la chirurg. Paris, 1845, torn. xv. (Atrophy of the deltoid 
in inflammation of the scapulo-humeral joint.) 

Lejeune. These de Paris, 1859. (Muscular atrophy after fractures.) 

Bezuel. These de Paris, 1864. (Muscular atrophy after acute articular rheuma- 
tism.) 

Ollivier. These d'agregation. Paris, 1869. (Muscular atrophy produced re- 
flexly by joint affections.) 

Baeckel. Effets de la coxalgie sur la croissance. Atch. de Phys., iZjo-'yi, p. 

435- 

Desnos et Barie. Progr. med., 1875, p. 557. (Muscular atrophy after trauma- 
tism.) 

Paget, James. Clinique chirurg., 1877. 

Boquet. These de Paris, 1877. 

Debove. Progr. med., 1880, p. loir. 

Guichard. These de Bordeaux, 1881. 

Charcot. Prog, med., Juin-Juillet 1882. 

Mondan. Recherches experimentales et cliniques sur les atrophies des mem- 
bres. Valence, 1882. 

Deschamps. Contribution a l'etude des atrophies musculaires a distance, appel- 
lees encore, " atrophies reflexes." These de Paris, 1883. (The trophic 
force of the nerve centres is diminished according to him.) 

Cornillon. Progr. med , 1883, xi, 21, p. 405. (Muscular atrophy after attacks 
of gout simulating progressive muscular atrophy.) 

Striimpell. Munch, med. Wochenschr., 1888, 13. (Muscular atrophy after 
acute articular rheumatism.) 

B. Diseases of the Trophic and Vaso-motor Nerves. 

In spite of the epoch-making - labors of Samuel (cf. lit.), who, 
after Romberg-, was the first to postulate the existence of defi- 
nite " trophic " nerve fibres for the regulation of the nutrition 
of the tissues, we are to-day still unable to demonstrate such 
fibres, nor do we know whether there exist purely trophic 
centres, or whether the trophic influence is exerted by some 
centres already well known — viz., by the motor, sensory, or 
vaso-motor. On the other hand, the existence of such a direct 
trophic influence of the nervous system upon the tissues can 
not be called in question. Again, we can not as yet decide 
whether or not this influence, upon which the nutrition of the 
tissues normally depends, is different for different tissues — as 
indeed seems quite probable — and whether it has to be re- 
garded as acting by inhibition or rather by an active stimu- 
lation. 



394 



DISEASES OF THE SPINAL NERVES. 



Occasionally, besides the trophic we meet also with vaso- 
motor disturbances, which lead us to conclude that not only 
the vaso-constrictor, but also the less important vaso-dilator 
nerves may become affected. With their anatomical relations 
we are better acquainted than with those of the trophic nerves. 
At any rate we know that in the cerebrum and in the medulla 
oblongata vaso-motor centres do exist. In their further course 
the vaso-motor fibres are thought to pass through the lateral 
columns of the spinal cord and to leave it through the anterior 
roots, but this is not yet proven, nor can we accept the exist- 
ence of Goltz' vaso-motor reflex centres in the spinal cord 
without further investigation. 

The vaso-motor disturbances which we sometimes see in 
acute diseases— for instance, in typhoid fever (Money, Lancet, 
December 3, 1887) — are phenomena due either to a condition 
of paralysis or of irritation. In the former case we have red- 
dening of the skin with elevation of the temperature, a con- 
dition which may also appear either independently or in the 
course of functional neuroses. In 4 the latter we have marked 
pallor and coldness of the skin, associated with formication, 
subjective sensations of cold, as, for example, in the so-called 
anaesthesia lavatricum (cf. Hirt, Krankheiten der Arbeiter, 
1878, Part II, p. 100). Such disorders need, however, not 
always lead to trophic changes. It is rather probable, as 
Kopp thinks, that, if the latter occur, disturbances in the nu- 
trition of the vessel walls must have preceded them (cf. the 
work of Thoma, lit.). 

Sometimes vaso-motor and trophic disturbances may coex- 
ist as genuine complications. 

Of clinical importance is the fact that trophic changes may 
occur either by themselves or accompany other, central, cere- 
bral as well as spinal affections. This may be explained by the 
fact that in order to bring about alterations in the trophic influ- 
ences, it is not necessary to have a disease of the ganglionic 
cells or cell groups, which probably act as centres, but that 
pathological processes in the peripheral nerves may also have 
the same effect. Among the central affections, which, how- 
ever, may remain latent for a long time, so that one might be 
led to regard the trophic changes as independent affections, we 
must mention in the first place tabes, which we shall discuss in 
this connection later, and after this certain cerebral diseases 
due to changes in the vessels, such as apoplex}- with the acute 



DISEASES OF THE TROPHIC AND V A SO-MOTOR NERVES. 



395 



bedsore, of which we have spoken on page 233, and again dis- 
eases of the gray axis of the spinal cord (Jarisch), among others 
the " paralysie generale spinale anterieure subaigue " (Pitres et 
Vaillard, Prog, med., 1888, 35). To the diseases of the periph- 
eral nerves and the infectious diseases, in the course of which 
trophic disturbances may occur, we have already alluded. 

At present we can form no idea how many diseases, not 
only of the nerves and of the muscles, but also of other organs, 
we shall have to call " trophic " when we have once become 
better acquainted with the position of the trophic centres and 
fibres than we are now. For the present the term is restricted 
to a small number of affections, and it will suffice to say a few 
words about the most important among them, and first about 
the tropho-neu roses of the skin. 

Anomalies of secretion which have to do with the sebaceous 
as well as the sweat glands are not uncommon. It is well 
known that seborrhcea, for example, may occur after long- 
standing menstrual disturbances, chlorosis, anaemia, after over- 
exertion, or as a consequence of too great sexual excitement, 
masturbation, etc., especially in young individuals, whereas 
diminished secretion of the sebaceous glands, as found, for in- 
stance, in ichthyosis and in senile atrophy of the skin, is com- 
paratively rare. The purely nervous origin of this, as well as 
of hyperidrosis and anidrosis, can hardly be questioned. Hy- 
peridrosis is seen on one side alone or on both sides in central 
diseases — for instance, in some diseases of the medulla oblongata 
(Traube), of the spinal cord (spinal apoplexy, myelitis), and of 
the entire nervous system (tabes, hysteria). It also occurs 
reflexly (Raymond). The anidrosis appears in peripheral facial 
paralysis, in dementia paralytica, and in certain skin affections, 
such as psoriasis, lichen, and ichthyosis. 

Among the skin affections associated with exudation we 
have erythema nodosum, urticaria, and a disease probably akin 
to it, the angio-neurotic oedema (Quincke), which appears some- 
times quite suddenly on different parts of the body, the patient 
feeling otherwise perfectly well. Accompanying the menses 
cutaneous swellings of nervous origin have been described (E. 
Boerner, Volkmann'sche Sammlung klinischer Vortrage, 1888, 
xi, No. 312). Again, we have certain forms of eczema, prurigo, 
herpes zoster, and others, although the nervous origin of them 
is not established beyond doubt. As every one of these affec- 
tions presents in its development, in its clinical significance and 



396 



DISEASES OF THE SPINAL NERVES. 



in its treatment, so much that is by no means clear we deem 
ourselves hardly called upon to enter into a detailed description 
of them here. Some, as, for instance, the herpes zoster in the 
course of facial paralysis, have been mentioned above (cf. page 
89). Equally obscure is the origin of cutaneous haemorrhages 
— we only wish to recall the ecchymoses which occur in tabes 
after severe attacks of pain — of the pigment hypertrophies 
(e. g., in lepra), of the anomalies of cornification (keratosis and 
ichthyosis), of the naevus, which is said to be due to intra- 
uterine disease of the spinal ganglia, of the atrophic conditions 
of the skin (stria? and maculae atrophica?), of the so-called glossy 
skin (glossy fingers), of the pigment atrophies (vitiligo), of the 
atrophy of the hair, and the atrophies or deformities of the 
nails, changes which we meet with in the most varied nervous 
affections and under the most varied circumstances. 

An interesting angio-neurosis is the so-called night palsy, 
which has been described by Ormerod, Bernhardt, and others. 
It consists in numbness, pain, and a feeling of weakness occur- 
ring at night in the upper extremities. Distinct anaesthesia and 
actual paralysis are not present. Women are affected more 
frequently than men, and seem to be particularly prone to it at 
the menopause. 

LITERATURE. 

Samuel. Die trophischen Nerven. Leipzig, i860. 

Lustig. Zur Lehre von den vasomotorischen Neurosen. Inaug. Diss. Breslau, 
1875. 

Alexander. Lancet, 1881, i, 25, 26. 

Stiller. Wiener med. Wochenschr., 1881, 5, 6. 

Seeligmiiller. Ueber Hydrops articulorum intermittens. Deutsche med. Woch- 
enschr., 1880, 5,6. (Is by Seeligmiiller regarded as a vaso-motor neuro- 
sis.) 

Schwimmer. Die neuropathischen Dermatosen. Wien u. Leipzig, 1883. 

Weiss. Prager Zeitschr. f. Heilk., September 15, 1885, vi. 6. (Zoster cere- 
bralis.) 

Kopp. Die Trophoneurosen der Haut. Wien, 1886, Braumuller. 

Renault. Note relative des troubles trophiques exceptionels d'origine rhumatis- 
male. Gaz. hebd., 1887, xliii, 24. 

Raymond. Des ephidroses de la face. Arch, de neurol., 1888, 43, p. 51. 

Thoma. Ueber das Verhalten der Arterien bei Supraorbitalneuralgie. Deut- 
sches Archiv f. klin. Med., 1888, Bd. xliii, Heft 4, 5. 

Seguin. Boston Med. and Surg. Journ., October, 1888, cxix, 15. 

The so-called symmetrical gangrene of the fingers and toes 
(sclerodactyly) which was first described in 1882 by Raynaud, 



RAYNAUD'S DISEASE. ^gy 

and which has, after him, been called Raynaud's disease, comes 
on with the following symptoms : The fingers appear at times 
as if dead (" doigts de mort "), at another time they turn a dark- 
red color and burn violently. Gradually disturbances in nu- 
trition, at first only transitory, later permanent, develop and 
blebs form, which open, leaving a sore, which heals with loss 
of substance". The nails fall out and are not replaced, whole 
parts die, the necrosis being symmetrical on both sides, and 
none of the usual causes of gangrene — such as disease of the 
heart or of the blood-vessels, septicaemia, traumatism, etc. — 
are present. The disease is, however, very rarely met with in 
its full development, while lighter grades, in which we have 
only to deal with a transient spasm (or paralysis) of the vessels, 
especially in the hand, are not uncommon. In such instances 
the hands become bluish and icy cold, and we have a condition 
known as local asphyxia. Raynaud's disease may be con- 
founded with peripheral neuritis, ergotism, diabetes, and senile 
gangrene. It should, however, not be difficult to avoid such a 
mistake if we take into consideration the characteristic course 
of the disease and the absence of any of the ^etiological factors 
before mentioned. In the treatment repeatedly, favorable 
results have been obtained by bathing the hands in warm 
water and the application of alcoholic menthol solution with 
a camel's-hair brush. 

LITERATURE. 
Weiss. Ueber sogen. symmetrische Gangran. Zeitschr. f. Hellk., 1882, iii, p. 

233- 
Frantzel. Zeitschr. f. klin. Med., 1883, vi, 3, p. 277. 
Lutz. Bayr. arztl. Intell.-Bl., 1884, xxxi, 24. 
Schulz. Deutsch. Arch. f. klin. Med., 1884, xxxv, p. 183. 
Vulpian. Gaz. des hop., 1884, 9 
Lauer. Ueber locale Asphyxie und symmetrische Gangran der Extremitaten. 

• Inaug. Dissert. Strassburg, 1884. 
Pitres et Vaillard. Arch, de Phys., January, 1885, 3me ser., v, p. 103. 
Hochenegg. Ueber symmetrische Gangran und locale Asphyxie. Wiener med. 

Jahrb., 1885, 4, pp. 569-658. 
Shaw. Raynaud's Disease. New York Med. Journ., December 18, 1886. 
Powell. Brit. Med. Journ., January 30, 1886, p. 203. 
Goldschmidt. Gangrene symmetrique et sclerodermic Revue de med., May, 

1887, p. 404. 
Wiglesworth. Peripheral Neuritis in Raynaud's Disease. Brit. Med. Journ., 

January 8, 1887. 
Potain. Gaz. des hop , July 26, 1887, lx, 90. 
Fox, R. Kingston. Lancet, December, 1888, ii, 25, 



393 



DISEASES OF THE SPINAL NERVES. 



Tannahill. Glasgow Med. Journ., December, 1888, xxx, 6. 
Bramann. Falle von symmetrischer Gangran. Deutsche Med.-Ztg., 1889,37, 
P- 432. 

Undoubtedly a close relation exists between Raynaud's dis- 
ease and scleroderma. In this latter very rare affection, which 
also depends upon trophic disturbances, the skin, after having 
presented cedematous swellings in the first stage, becomes later 
hard and immovable, so that it is impossible to pick up a fold 
of it between the fingers. The affected parts, more particularly 
the face, neck, and the upper portion of the chest, where fre- 
quently a diffuse increase in the pigment is noticeable, are im- 
peded in their movements, the play of the features is lost, the 
mouth can not be completely opened, the eyes can not be 
closed, and rotation of the head becomes impossible, etc. The 
patient feels a sensation of discomfort ; the coldness of the 
skin, which reminds one of that of a corpse, is most distressing, 
and a slight fall in the outside temperature is sufficient to bring 
about cyanosis. Quite gradually the atrophic, the terminal 
stage comes on, in which the skin gets as thin as paper, remain- 
ing, however, firmly fastened to the underlying tissues, so that 
it is still impossible to pick up a fold. With these changes is 
associated an atrophy of the muscles, which has to be regarded 
partly as a tropho-neurosis, partly as an atrophy due to inac- 
tivity, and the patient becomes helpless and unfit for work. 
After the disease has lasted for several years, if convalescence 
has not set in in the second stage, a general marasmus develops 
which leads to a fatal issue. An effectual treatment is not 
known. Warm baths, simple ointments, the constant current, 
internally tonics, iron, cod-liver oil, etc., may be tried, but we 
are not justified in placing any confidence in them. 

Very closely related to scleroderma is a disease which fif- 
teen years ago was for the first time described by the English- 
men Gull and Ord under the name of myxcedema, and later 
by Charcot under the name of cachexie pachydermique, an affec- 
tion which only in quite recent years has attracted attention 
in Germany. 

The beginning of the disease shows itself by a peculiar 
swelling of the whole face, the skin, especially of the eyelids 
and the cheeks, appearing cedematous. The lips are not com- 
pletely closed and the saliva dribbles from the corners of the 
mouth. The face becomes, owing to the stumpy thick nose 



MYXCEDEMA. 



399 



and half-opened eyes, somewhat uncouth and common, then 
expressionless and cretin-like (cf. Fig. 137). The patients, es- 
pecially if they are females, grow to look so much alike that 
they appear as if they all belonged to the same family. The 
color of the face is pale, the skin is wax-like, but does not pit 
on pressure. The oedema of the rest of the body has the same 
character as that of the face. The skin of the neck forms folds, 
the hands are thickened. On the hard wrinkled skin circum- 
scribed thickenings can be seen, hair and nails fall out, the 




F 'g:- 137.— Case of Myxcedema. (After Charcot.) 

teeth become carious, the secretions diminish and dry up. 
Amenorrhcea is common. Lungs, heart, and the large vessels 
present no abnormities. On examination the urine is found 
to be negative, while the temperature is subnormal. Among 
the concomitant symptoms must be mentioned sensory and 
motor disturbances, uncertainty in the gait, and general lassi- 
tude. Such patients get easily fatigued, their mental faculties 
suffer, and a condition of beginning imbecility develops. 

The pathogenesis and the anatomical seat of the disease are 
quite obscure. It is generally accepted that the swelling is not 



400 



DISEASES OF THE SPINAL NERVES. 



an oedema, but is due to the formation of a myxomatous new- 
growth containing mucin. Mucin has been found in great 
quantities in the skin, the connective tissue, the blood, and the 
saliva of these patients. We seem to be justified in assuming 
that the thyroid gland has a good deal to do with myxcedema, 
since in most instances after the extirpation of this gland 
symptoms of myxcedema appear, and where this was not the 
case it is possible that either accessory thyroid glands existed, 
or that the removal was not complete. The operations on 
men and monkeys (Horsley) which have so far been performed 
seem to give no support to the idea that the true cause of this 
is to be sought for in injury of the trachea, of the recurrent 
laryngeal nerve, or of the cervical sympathetic. In the cases 
in which operative measures are not concerned we have to 
deal with a degeneration of the thyroid gland, the normal 
glandular tissue becoming replaced by a delicate fibrous tis- 
sue. The cause of such a degeneration is entirely obscure. 
The few instances in which just before the onset the patient 
had gotten a thorough drenching in the course of his daily 
work afford no sufficient grounds for looking upon this as an 
^etiological factor. 

The researches recently published by Munk (cf. lit.) indi- 
cate that after all we are justified in being doubtful whether 
the symptoms appearing after extirpation of the thyroid are 
actually due to the loss of the gland, or whether they have to 
be regarded as a consequence of the operation itself. Accord- 
ing to him, it is not as yet settled that the thyroid gland itself 
possesses important vital functions which are of great signifi- 
cance to the central nervous system. 

We are not likely to mistake the affection for any other ; 
still attention has been called to the fact (Lassar) that certain 
chronic erysipelatoid swellings may give to the face a similar 
expression to that seen in myxcedema. Among those affected 
with the disease observed up to the present time the majority 
were women and middle-aged. We are not yet acquainted 
with any treatment, nor has any been tried so far as we know. 

LITERATURE. 

Gull. On a Cretinoid State supervening in Adult Life in Women. Transact, of 
the Clin. Soc, 1874, vii, p. 180. 

Ord. On Myxcedema. Med.-chir. Transact., 1878, Ixi, p. 57. 

Hammond. On Myxcedema, with Special Reference to its Cerebral and Nerv- 
ous Symptoms. Neurcl. Contribut., 1886, i, 3, p. 36. 



HEM I A TR OP HI A FA CIA LIS. 



40I 



Charcot. Gaz. des hop., 1881, 10. 

Saville. Case of Myxoedema in a Male. Brit. Med. Journ., December 3, 1887, 

p. 1216. 
Paton. Glasgow Med. Journ., December, 1887. 
Reverdin. Contribution a l'etude du myxcedeme consecutif a l'estirpation totale 

ou partielle du corps thyroi'de. Revue med. de la Suisse rom., 1887, 5, 6. 
Zielewicz. Berl. klin. Wochenschr., 1887, 22. 
Munk. Untersuchungen iiber die Schilddriise. Sitzungsberichte der konigl. 

preuss. Akad. d. Wissenschaften, 1888. 
Probnik. Die Folgen der Exstirpation der Schilddriise. Archiv f. experim. 

Pathol, u. Pharmakol , 1888, xxv, 2. 
Conclusions of the Myxoedema Committee. Brit. Med. Journ., June 2, 1888, p. 

1 162. 
Mosler. Ueber Myxodem. Virchow's Archiv, Bd. 114, Heft 3. 
Cousot. Idiotie avec cachexie pachydermique. Bull, de la Societe mentale de 

Belgique, 1888, 51. 
Manasse. Berl. klin. Wochenschr., 1888, 47. 

The next affection to which we shall call attention is as re- 
markable as it is rare. According to our present ideas, it has 
also to be ranked among the tropho-neuroses. We are refer- 
ring to a very gradually developing atrophy of the face (some- 
times ushered in by pain and parassthesias), which may appear 
on one or both sides, and generally embraces equally the skin, 
the subcutaneous tissue, the muscles, and the bones. The begin- 
ning is usually as follows : Whitish spots appear on the skin of 
the face, which sink in more and more and are accompanied by 
a diminution of the fatty tissue below ; gradually the atrophy 
increases in extent, and nothing escapes with the exception of 
the musculature, and this only occasionally and for a certain 
time. The affected side is sunken in and the skin assumes a 
whitish-brown discoloration. The bones, especially the upper 
jaw, and with it the teeth, atrophy ; the latter fall out as well 
as the hair, which often appears of a light color or distinctly 
gray. The bone atrophy is the more marked the younger the 
patient at the onset of the disease (Virchow). If the disease is 
confined to one side only — hemiatrophia facialis — the median 
line forms a sharply defined border and the diagnosis is very 
plain. If both sides are affected, as happened in Eulenburg's 
case after measles (Lehrb. der Nervenkrankh., 1878, ii, p. 620), 
it may be more difficult to recognize the affection. The grooves- 
and furrows which are found in the face greatly disfigure it 
(Fig. 138). The corresponding half of the tongue becomes 
small and often presents gap-like retractions, such as we de- 
scribed in hemiatrophy of the tongue (Fig. 119). Among the 
26 



402 



DISEASES OF THE SPINAL NERVES. 



muscles, not only those supplied by the facial, but also those 
supplied by the trigeminus, are implicated. The extension of 
the atrophic process to the neighboring shoulder and even to 
the upper arm is not unusual. Sensibility is not altered in the 
affected region. 

Most of the few cases observed clinically have never come 
to autopsy. Of great interest, therefore, was the result of an 
examination, which Mendel was enabled to relate before the 
Berlin Medical Society, on such a patient who had died of 




Fig. 138.— Hemiatrophy Facialis (personal observation). 



phthisis, and who had previously been examined by Romberg 
and later on by Virchow (Deutscher Med.-Ztg., 1888, xxxiii, p. 
407). On examining the origin of the trigeminus all the other 
roots were found to be normal ; only in the descending root 
could atrophic changes be recognized, a fact which would in- 
dicate that the trophic fibres must be contained therein. 

Other observations (Ruhemann) also point to a very inti- 
mate connection between facial atrophy and the trigeminus ; 
however, more post-mortem observations confirmatory of those 
of Mendel are needed to clear up the pathology of the disease. 



ACROMEGALY. 4 3 

Of the astiology little that is positive is known. Age and 
sex seem to have little influence. The disease has been known 
to occur at all times of life and also to be congenital ; it has 
been observed in both sexes. According to Lewin, the fre- 
quency with which the two sexes are attacked is in the ratio of 
six males to nine females. Hereditary predisposition is cer- 
tainly not a conditio sine qua non, because there are cases — among 
others, the one I have reported myself — in which the patients 
belonged to quite healthy families. Sometimes it has happened 
that the atrophy was preceded by other nervous affections — 
trigeminal neuralgia, migraine, epilepsy, etc. — but this is by no 
means the rule. In a few cases the disease has followed in- 
juries about the face or of the cervical sympathetic (Seelig- 
miiller); more frequently no cause whatever could be demon- 
strated, and it was impossible to make any conjecture as to the 
astiology. The outlook for recovery is absolutely bad, and 
therapeutics, so far as our knowledge goes, is powerless. 

LITERATURE. 

Eulenburg. Ueber progressive Gesichtsatrophie und Sclerodermie. Zeitschr. f. 

klin. Med., 1882, v, 4. 
Wolff, J. Virchow's Archiv, 1883, xciv, 3, p. 393. 
Putzel. A Case of Progressive Facial Hemiatrophy. The Med. Rec, April 16, 

1887. 
Barwise. Lancet, December 31, 1887. 
Herz. Archiv f. Kinderheilkunde, 1887, viii, p. 241. 
Lowenfeld. Ueber einen Fall halbseitiger Atrophie der Gesichts- und Kaumus- 

culatur. Miinchner med. Wochenschr., 1888, xxxv, 23. 
Mendel. Ueber Hemiatrophia facialis. Deutsche Med.-Ztg., 1888, 33. 
Ruhemann. Deutsche med. Wochenschr., 1889, 3, 55. 

Under the name of acromegalia {aicpov, extremity) Marie de- 
scribed, in 1886, a peculiar non-congenital hypertrophy of the 
hands, feet, and head, to which affection attention had been 
drawn before him by Fritsche and Klebs (cf. lit.). The extrem- 
ities appear increased in length as well as in breadth. The 
bones of the face, especially those of the cheeks and the lower 
jaw, present considerable enlargement (cf. Figs. 139 and 140), 
and the measurements of the skull are above normal. In the 
same way the lips, ears, nose, and tongue are found enlarged, 
whereas all the muscles are feeble. The skin appears yellowish 
and pale, but is otherwise normal. The thyroid gland was 
almost always atrophic in the cases observed up to the present 



404 DISEASES OF THE SPINAL NERVES. 

time. In spite of their gigantic appearance the patients are 
feeble and without strength. The sexual functions are lost 
early and completely (Freund, cf. lit.). 

The onset of the disease dates back to early childhood, 




Fig. 139. —Case of Acromegaly. (After P. Marie.) 

and it has to be regarded as an abnormity in development 
(Freund) " which, probably beginning as early as the cutting 
of the second teeth, certainly sets in energetically at the 
period of puberty, and consists in a rapidly developing en- 
largement of the facial part of the skull, which by far exceeds 
the physiological limits of growth. This increase is especially 
marked in the lower jaw and also in the extremities, with their 
girdle attachments, while the rest of the skull and the trunk 
are only secondarily altered." 

Only three cases have come to autopsy since Marie's work 
appeared. In one published by Frantzel (cf. lit.), congenital 
smallness of the aorta, with atrophy of the right ventricle, was 
noted. The second is reported by Broca (cf. lit.), w*ho in his 
account chiefly occupies himself with a description of the hy- 
pertrophy of the ends of the bones ; and a third by Saundby 
(cf. lit.). " 

About the cause of acromegalia just as little is known as 



ACROMEGALY. 405 

about its treatment. According to Goldscheider, who estab- 
lished the fact that the giant growth is not confined to the dis- 
tribution of any one nerve — being found, for instance, in the 
hand, in that of the musculo-spiral and median, more rarely 




Fig. 140.— Case of Acromegaly. (After P. Marie.j 

in that of the ulnar — the ^etiological influence of the trophic 
nerve-fibres is still a matter of doubt. 

LITERATURE. 

Fritsche u. Klebs. Beitrag zur Pathologie des Riesenwuchses. Leipzig, 

1884. 
Marie. Sur deux cas d 'acromegalic Revue de med., 1886, iv, 4, p. 297. 
Frantzel, O. Deutsche med. Wochenschr., 1888, 32. 
The same. Deutsche Med.-Ztg., 1888, 48, p. 581. 
Erb. Deutsches Archiv f. klin. Med., February 4, 1888, Bd. 42. 
Broca. Un squelette d'acromegalie. Archives gener. de med., December, 

1888. 
Adler. Boston Med. and Surg. Journ., November 21, 1888, cxix. 



406 DISEASES OF THE SPINAL NERVES. 

Freund, V. A. Ueber Acromegalic Volkmann'sche Sammlung klin. Vortrage, 
1889, 329, 330 (11. Ser., Heft 29, 30). (Contains older references.) 

Virchow. Ein Fall und ein Skelett von Acromegalic Berl. klin. Wochenschr., 
1889, 5. 

Goldscheider. Archiv f. Anat. u. Physiologic Physiol. Abtheilung, 1889, 1, 2. 

Saundby. Acromegaly. Brit. Med. Journ., January 5, 1889. 

Marie, P. L' Acromegalic Etude clinique, Paris, 1889. 

Appendix. — Diseases of the Muscles — Primary Myopathies. 

Diseases of the muscles, which consist in alterations in 
their volume (which is generally diminished, less frequently 
increased), and consequent disturbances of function, may occur 
under the most varied conditions. They may be produced 
by cerebral affections, as we have pointed out on page 233, 
where we spoke of the possibility of an affection of trophic 
centres in the cortex ; they may be the result of spinal diseases, 
as we shall later find out in discussing syringomyelia and pro- 
gressive muscular atrophy, but they may also — and this is 
what interests us here more especially — occur independently 
of any central disease as primary myopathies. 

Considered from an anatomical standpoint, this disturbance 
in the nutrition of the muscles, the dystrophia muscularis pro- 
gressiva of Erb, the myopathia progressiva primitiva of Charcot, 
consists either in a diminution, a wasting of the muscular tissue, 
owing to which the volume of the part affected becomes smaller ; 
or during the pathological process there may come about an in- 
crease in volume, which is either due to an actual increase and 
abnormal growth of the muscles — a genuine muscular hyper- 
trophy — or to a growth of the interstitial fatty tissue, in which 
latter case we speak of a pseudo-hypertrophy of the muscles. 
Sometimes both conditions are found in one and the same indi- 
vidual, so that certain muscles appear atrophied, while others, 
in consequence of the simultaneous development of fat, appear 
strikingly large and hypertrophied. The microscopical exam- 
ination (Charcot, F. Schultze, Striimpell) shows considerable 
increase in the interstitial connective tissue between the indi- 
vidual fibres, which latter have retained their transverse stria- 
tion. The genuine hypertrophy which is seen in places must 
be regarded, according to Striimpell, as compensatory. 

About the aetiology of primary myopathies we know very 
little. It should, however, be mentioned that, according to all 
the observations made up to the present time, the} 7 belong en- 
tirely to eany life, developing as they do before the twentieth 



JUVENILE MUSCULAR ATROPHY. 407 

year. Heredity plays frequently a role in the disease, since not 
uncommonly several cases occur in the same family. Lesage 
has shown that they also may follow certain other diseases, as, 
for example, typhoid fever (cf. lit.). In such instances we 
have to deal with a secondary lipomatosis, developing in cir- 
cumscribed areas of the body, as the result of certain arterial 
changes. 

In our present state of knowledge we seem justified in as- 
suming that these myopathies occur regularly in certain groups 
of muscles, so that different " types " can be distinguished, and 
that on the whole the upper half of the body, more particu- 
larly the upper extremities, are more often and more severely 
attacked by the pathological process than the lower parts, 
and more especially than the legs. It is important always 
to observe whether the face remains intact or not, as in the 
former case we are dealing with the hereditary muscular atro- 
phy which Erb has described as the " juvenile form " ; in the 
latter, with the form which Landouzy and Dejerine have de- 
scribed, and which has by them been called " myopathic atro- 
phique progressive." 

The so-called " juvenile muscular atrophy " which develops 
in early youth, more often in boys than in girls, attacks by 
preference the pectorales, the trapezius, the latissimus dorsi, 
the serratus magnus, the rhomboidei, the sacro-lumbalis, and 
the longissimus dorsi, while the majority of the muscles of the 
forearm, the sterno-cleido-mastoideus, the levator anguli scapu- 
las,, the coraco-brachialis, the teretes, the deltoid, the supra- 
spinatus and infraspinatus, remain, as a rule, intact. The small 
muscles of the hand, which in spinal atrophy become affected 
so early and in such a typical manner, are here not implicated 
(Fig. 141). It is hardly necessary to enter into a description of 
the disturbances of function which necessarily must result from 
disease of so many muscles. If we remember how much im- 
paired are the movements of the arm, which can not be raised 
above the horizontal position, etc., we can understand the 
gravity of the child's affliction. If, as in the long course of 
the disease not uncommonly happens, the process extends to 
the lower half of the body, the glutei, the peronei, the quadri- 
ceps, and tibialis anticus become implicated and the patients at 
first walk with an uncertain gait, then waddle in a character- 
istic manner, and finally lose the use of their legs. The impli- 
cation of the muscles supplied by the bulbar nerves, which has 



4o8 



DISEASES OF THE SPINAL NERVES. 



been observed by Bernhardt (cf. lit.), of course has a very de- 
cisive influence upon the duration and course of the disease. 

Fibrillary twitchings in the affected muscles, as we see it so 
commonly, we may say regularly, in the so-called progressive 





Fi g< I4 i._ Erb's Juvenile Muscular Atrophy. (After Marie and Guinon.) 

muscular atrophy (spinal), is here wanting with the same regu- 
larity. Neither can any changes in the electrical excitability 
be demonstrated, with the exception, of course, of a diminution 
due to the disappearance of a more or less large number of 
muscle fibres. The course of the disease is, as we said, emi- 
nently chronic. It may extend over a space of twenty or thirty 



PROGRESSIVE ATROPHIC MYOPATHY. 



409 



years, since bulbar symptoms occur but rarely and we can 
only look for a fatal issue if the process involves the diaphragm 
and respiratory disturbances result. The diagnosis never pre- 
sents any difficulties. After careful examination, taking into 
account the distribution of the atrophy, the onset of the disease 
in early life, with the fact that more than one member of the 
family is affected, the long duration of the disease, the absence 
of fibrillary twitchings, we can not mistake the myopathic for 
the spinal form. The treatment must consist chiefly of good 
care and nursing. All attempts to arrest the process by the 
application of electricity or the use of massage, baths, or in- 
ternal medicines, have proved to be of no avail. 

The facio-humero-scapular type of muscular atrophy of 
Landouzy and Dejerine, the " progressive atrophic myopathy," 
a form which had, however, already been described by Du- 
chenne under the name of " progressive muscular atrophy of 
infancy," begins in the muscles of the face, and before any other 
symptoms make their appearance our attention is attracted by 
the listless, sleepy expression of the face, the smooth forehead, 
the faulty movements of the mouth, the inability to whistle and 
to keep the lips together. At the same time there is a condi- 
tion of lagophthalmus, so that the patient in spite of the great- 
est exertion is unable to shut his eyes (cf. Fig. 142). Gradually 
the muscles of the upper extremities and the trunk become af- 
fected in almost the same distribution as in the juvenile paraly- 
sis. The course is the same in both these forms. Here also 
there are no fibrillary twitchings and no changes in the elec- 
trical excitability, and although the pseudo-hypertrophy of the 
muscles, which we shall presently describe, is not uncommon 
in the juvenile form and is here never present, there is no ques- 
tion but that the two affections are identical and that only in 
some cases, from reasons not as yet understood, the interstitial 
connective tissue becomes early increased, while in others 
nothing else can be demonstrated but simple atrophy, with in- 
crease in the number of muscle nuclei and here and there the 
formation of vacuoles in the fibres. The diagnosis is so much 
facilitated by the "myopathic facies " — that is, the expression 
produced by the sinking in of the cheek, the somewhat depend- 
ent lower lip, and the inability to close the eyes — that the ex- 
perienced diagnostician is frequently able to recognize the 
disease at the first glance. Marie and Guinon have called 
attention to the possibility of confounding the disease with 



4io 



DISEASES OF THE SPINAL NERVES. 



lepra anassthetica, in the course of which also weakness of the 
facial muscles exists (cf. lit.). It is interesting to note in this 
connection that sometimes disturbances of function in the facial 
muscles may constitute a congenital defect which under cer- 
tain circumstances may be followed by an actual atrophy ; 




Fig. 142. — Progressive Atrophic Myopathy. Inability to close the eyes completely. 
(After Marie and Guinon.) 



further, that in sisters or brothers of individuals who suffer 
from this myopathy which we have just described, a certain 
imperfection in the development of the facial muscles may be 
found, although the disease never breaks out in them. These 
are facts which Striimpell especially has pointed out, but the 
cause remains still wholly unexplained. About the treatment 
we need add nothing to what we have said with reference to 
the juvenile form. 

The third form of the muscular diseases now under consid- 
eration — the so-called pseudo-hypertrophy — is connected with 
an increase in the interstitial adipose tissue which, in spite of 
the atrophy of the muscle fibres, leads to an apparent increase 
in the volume of the affected parts. The disease was known 
and described by Griesinger in 1864, and again by Duchenne in 
1868. It begins generally in the muscles of the trunk and at- 
tacks, in contradistinction to the two forms just described, by 
preference the lower parts of the body, the muscles of the back, 



PSEUDO-HYPERTROPHIC MUSCULAR ATROPHY. 



411 



loins, and thighs. Though for a long time the patient can use 
his arms and hands just as well as usual, the walk, owing to the 
affection of the erector muscles of the spine, becomes altered 
in the characteristic manner which we have described on page 
363. The condition of the patient may 
remain unchanged for years before the 
arms also take part in the process. When 
this happens it occurs in the same man- 
ner as in the juvenile form. The diag- 
nosis is very much facilitated by the ap- 
pearance of the patient. The enlarge- 
ment of the calf muscles, the thighs, and 
the glutei (which are sometimes colossal), 
give to him the appearance of a giant 
and suggest a supernatural strength (cf. 
Fig. 143); but the fact that these great 
masses feel spongy and soft, and that 
the electrical excitability is consider- 
ably decreased owing to the diminution 
in the number of the muscle fibres, read- 
ily explains why these sturdy-looking 
persons are feeble and without strength 
and as good as deprived of the use of 
their limbs. 

In its onset the disease resembles 
closely the other forms. Here also only 
children become affected ; more especially 
those between the ages of four and nine. 
Here also the disease may occur in sev- 
eral members of the same family, so that 
we must undoubtedly assume a heredi- 
tary predisposition, and here also the 
fibrillary twitchings are not met with. 
Duration and treatment are the same as in the juvenile atrophy 




PSEUEO- HYPER- 
TROPHY of the Muscles 
of the Legs with Atro- 
phy of the Muscles of 
the Back. (After Du- 

CHENNE.) 



Congenital atrophy of the muscles may be found in cases of 
malformation of the arms and hands. Fig. 144 represents a 
boy aged thirteen in whom the forearms are absent; some of 
the fingers are grown together and some deformed. A similar 
case has been reported by Wilkin (Lancet, page 1265, Decem- 
ber 14, 1887), where there was atrophy of the biceps and the 
brachialis anticus. 



412 



DISEASES OF THE SPINAL NERVES. 



Absence of certain individual muscles is rarely observed. 
Erb has recently reported a case in which there was an almost 
entire absence of both trapezii (Neurolog. Centralbl., i, 1889). 
Among earlier instances the pectorales (Ziemssen), the biceps 
(McAllister), the deltoid, and gastrocnemius (Gruber), were 
wanting. These cases possess no clinical interest. 

The sensory disturbances which are peculiar to the mus- 
cles, but about the exact anatomical nature of which we know 




Fig. 144.— Absence of the Forearms. The fingers are partly grown together. Atrophy 
of the muscles of the upper arms (personal observation). 



nothing, are called myalgias or muscular rheumatisms. ^Etio- 
logically, overexertion, strains (possibly rupture of certain mus- 
cle fibres which may happen during gymnastic exercises or 
other violent bodily exertion), must be mentioned in this con- 
nection. Sometimes we are unable to find any such cause, 
and we have to attribute the trouble to the influence of cold. 
There are persons who for years or tens of years suffer from 
myalgic pains which come and go and may disappear for 



MYALGIAS. 



413 



certain periods of time completely, and it is just possible that 
chronic intoxications — e. g., alcoholism, perhaps also circu- 
latory disturbances — have a predisposing- influence. Among 
such myalgias, which may be very painful, even sufficiently 
so as to interfere with the occupation of the patient for a 
longer or shorter period of time, we have, for instance, the 
torticollis rheumatica, in which the muscles of the neck, the 
myalgia lumbalis (lumbago), in which the muscles of the loins, 
the myalgia intercostalis, in which the intercostal muscles are 
attacked. The shoulder muscles may also be affected, and the 
myalgia in this region may become very obstinate without any 
implication of the brachial or cervical plexuses being demon- 
strable. In the diagnosis we must think of the possibility of 
an implication of the nerves and endeavor to exclude neuralgia. 
We must further remember that central diseases may give rise 
to muscular pains. The inexperienced may mistake the lanci- 
nating pains of tabes for chronic muscular rheumatism, and 
thus obscure the correct diagnosis for years. It will hardly 
be difficult to avoid confounding - muscular rheumatism with 
articular rheumatism if we take into consideration the general 
condition of the patient, the appearance of the joints, the tem- 
perature, pulse, etc., which in the former affection remain 
normal. 

In the treatment we should, first of all, endeavor to detect 
any underlying cause, and, if such exists, remove it. In re- 
cent cases, besides subcutaneous injections of morphine, sali- 
cylic acid may be tried internally ; yet we should not spend 
much time with it if we perceive no effect, but should rather 
prefer local applications — irritants to the skin, poultices, mus- 
tard plasters, liniments, also massage and electricity — especially 
if the affection remains localized. If this is not the case, but if 
the pains travel round the body and the course assumes a 
more chronic type, treatment by sweating, steam baths, also 
mud baths or baths of Pinus silvestris, the non-medicated hot 
springs (Gastein, Johannisbad, Teplitz) or the sulphur springs, 
among others Pistyan, in Hungary, will be recommended. As 
a last resort, we may advise the patient to go to a well-con- 
ducted hydrotherapeutic establishment (Grafenberg, Kalten- 
leutgeben, Nassau, etc.). 



4 i4 DISEASES OF THE SPINAL NERVES. 



LITERATURE. 

Landouzy et Dejerine. De la myopathie atrophique progressive. Revue de 

med., February, March, 1885 
Marie et Guinon. Formes cliniques de la myopathie progressive primitive. Ibid., 

October, 1885 
Westphal. Ueber einige Falle von progressiver Muskelatrophie mit Betheilig- 

ung der Gesichtsmuskeln. Charite-Annalen, 1885. 
Charcot. Revision nosographique des atrophies musculaires progressives. Progr. 

med., March 7, 1885. 
Mossdorf. Neurol. Centralbl., 1885, iv, 1. (Implication of the facial muscles in 

the juvenile muscular atrophy.) 
Krecke. Miinchner med. Wochenschr., 1886, xxxiii, 14-16. (Implication of 

the facial muscles in muscular atrophy.) 
Vulpian. Maladies du systeme nerveux, 1886, torn, ii, p. 436. 
Ladame. Contribution a 1'etude de la myopathie atrophique progressive. Revue 

de mid., October, 1886. 
Landouzy. Note sur le facies myopathique et sa valeur dans la semiotique de 

l'enfant et de l'adult. Bull, de la Societe med. des hop., October, 1886. 
Charcot et Marie. Surune forme particuliere d'atrophie musculaire progressive, 

souvent familiale, debutant par les pieds et les jambes et atteignant plus 

tard les mains. Revue de med., 1886, vi, 2, p. 97. 
Landouzy et Dejerine. Nouvelles recherches sur la myopathie atrophique pro- 
gressive etc. Revue de med., December, 1888. 
Lichtheim. Ueber hereditare progressive Muskelatrophie. Schweizer. Corr.- 

BL, 1888, xviii, 19, p. 603. 
Hitzig. Berl. klin. Wochenschr., 1888, 34, 35. 
Bernhardt. Ueber eine hereditare Form der progressiven spinalen, mit Bulbar - 

paralyse complicirten Muskelatrophie. Virchow's Archiv, 1888, Bd. 

115. 2. 
Lesage. Note sur une forme de myopathie hypertrophique secondaire a la 

fievre typhoide. Revue de med., 1888, viii, 11, p. 903. 
Sachs. Progressive Muscular Dystrophies, journal of Nerv. and Ment. Dis- 
eases, November, 1888, xiii, 11. 
Stern. Ein Fall von progressiver Muskelatrophie (juvenile form, Erb), mit halb- 

seitiger Betheiligung des Gesichtes. Mittheil. aus d. med. Klinik in Komgs- 

berg. Leipzig, Vogel, 1888. 
Lorenz, A. Die Contracturen des Kniegelenks bei Ouadricepslahmungen. 

Wiener klin. Wochenschr., 1888, i, 37. 
Lichtheim. Ueber hereditare progressive Muskelatrophie. Centralbl. f. Ner- 

venheilk., 1888, xi, 20. 
Souza, Antonio Veiga de. Zwei Falle von juveniler Form der Muskelatrophie. 

Inaug. Diss., Kiel, 1888. 
Troisier et Guinon. Deux nouveaux cas de myopathie progressive primitive 

chez le pere et la fille. Revue de med., 1889, ix, 1. 
R£mond. Une observation d'atrophie musculaire myelopathique a type scapulo- 
humeral. Progr. med., 1889, 2. 
Sperling. Neurolog Centralbl., 1889, 3. 



PRIMARY MYOPATHIES. 455 

Winkler en van der Weyde. Primaire myopathic (type facio-scapulo-humerale) 

gecombineerd med. ophthalmoplegia progr. superior. Nederl. Weekbl., 

1889, i, 3. 
Scheuthauer. Histol. Untersuchung eines Falles von Pseudohypertrophic der 

Muskeln. Archiv f. Psych, u. Nervenkrankh., 1889, xx, 2. 
Hoffmann. Ueber progressive neurotische Muskelatrophie. Ibid., 1889, xx, 3. 
Herringham. Muscular Atrophy of the Peroneal Type affecting many Members 

of a Family. Brain, 1889, xi, p. 230. 
Pal. Ueber einen Fall von Muskelhypertrophie mit nervosen Symptomen. 

Wiener klin. Wochenschr., 18S9, ii, 10. 



PART III. 

DISEASES OF THE SUBSTANCE OF THE SPINAL 
CORD. 

Diseases confined to the substance of the spinal cord are 
rarer than those of the brain substance. The cause of this may 
lie in the fact that not only are the vessels of the spinal cord 
actually less frequently the seat of disease than those of the 
brain, but also that when they become diseased the conse- 
quences entailed are generally not of so grave a nature as 
those resulting from lesions of the cerebral vessels. 

As in cerebral diseases, here also two questions must ever 
be kept in view by the physician : (i) Where is the spinal lesion 
situated ? (2) What is its nature ? As we shall see later, it is 
especially the second which is of importance for the prognosis 
and choice of treatment. Both, however, are of equal weight 
for the proper recognition and conception of a given case. As 
in the study of the brain lesions, the topical and pathological 
diagnosis should here no less go hand in hand. 

I. Consideration of Spinal Diseases with Reference to 
their Seat — Topical Diagnosis. 

As a thorough acquaintance with the anatomy of the parts 
is of the highest importance in making a topical diagnosis, 
some remarks on these points may in this place not be unwar- 
ranted. 

Without being separated by any sharp line of demarcation from 
the medulla oblongata, the spinal cord extends from the upper mar- 
gin of the arch of the atlas to the first lumbar vertebra, where it 
ends in the conus medullaris. From this point it is seen as a long 
filiform continuation — the filum terminale. The cauda equina con- 
sists of the longitudinal nerve bundles which accompany the filum 
terminale, and corresponds to the lumbar and sacral part of the 
vertebral column. As it is apparent that the different pairs of nerves 



ANA TOMICAL RELA TIONS. 



417 



C.l 



6c 

70 



2 

3 



8 



9$2 
10 

11 i% 
12, 



do not leave the spinal cord at the level of 
the vertebrae after which they are named, 
but that they must necessarily do so higher 
up, it is important to know to what nerves 
certain parts of the vertebral column cor- 
respond. Thus we must remember that the 
first three cervical vertebrae correspond to 
the origin of the third, fourth, and fifth cer- 
vical nerves, and that the seventh cervical 
vertebra corresponds to the first dorsal 
nerve. The spinous process of the fifth dor- 
sal vertebra corresponds to the origin of 
the seventh, that of the tenth to the twelfth 
pair of dorsal nerves. Opposite the eleventh 
dorsal vertebra originates the first, between 
the eleventh and twelfth the second, oppo- 
site the twelfth the third and fourth lumbar 
nerves. Between the twelfth dorsal and 
first lumbar vertebra the fifth lumbar and 
first sacral nerves take their origin, the 
other sacral nerves opposite the first lum- 
bar vertebra. The cervical enlargement 
corresponds, therefore, to the spinous pro- 
cesses of the cervical vertebrae, the lum- 
bar enlargement to the spinous processes 
of the last dorsal vertebrae. All these re- 
lations, and, moreover, the fact that the 
spinous processes, which alone can- be our 
guides, are not always on the same level 
as their corresponding vertebrae, are demon- 
strated in Fig. 145 j 

The relation between the white matter 
and the gray which it incloses becomes 
apparent in a transverse section of the spi- 
nal cord. Here we see also that an ante- 
rior and a posterior fissure divide the spi- 
nal cord into two halves. These fissures, 
however, do not meet, but are separated 
from each other by the so-called " commis- 
sures " which connect the two halves of the 
cord. The anterior part of the gray mat- Fig. i 4S .— The Relations of 
ter, the so-called "anterior horn," does not the Origin of the Nerves 
present the same diameter and form through- TO THE BoDIES OF ™ E Ver " 

V fe TEBR.E AND THE SPINOUS 

out, and in the cervical and lumbar en- processes. (After Gowers.) 
27 



L.l 
2 



(M 












4i: 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



largement is larger than in the dorsal part of the cord (cf. Fig. 147). 
From this anterior horn proceed the anterior nerve roots and pass 
through the white matter which lies externally. The posterior horn 
is much smaller and extends almost to the entrance of the posterior 

roots, which reach it after passing 
through the external part of the 
posterior columns (" root zone " 
of Charcot). The arrangement of 
the white substance and its sub- 
division into columns and tracts is 
determined (1) by the existence of 
the above-mentioned fissures, (2) 
by the entrance of the nerve roots, 
(3) by the shape of the gray mat- 
ter. We distinguish roughly an 
" antero-lateral column" and a 
" posterior column " on each side. 




d c 
Fig. 146.— Scheme of the Conducting 
Paths in the Spinal Cord at the 
Level of Fifth Dorsal Nerve. (After 
Flechsig.) va,, anterior, hw, posterior The former contain (a) the crossed 
root, a, direct, g, crossed pyramidal lateral or pyramidal tracts (cf. 

tracts. *, anterior column ground bundle. page lg g\ n\ the direct Cerebellar 

c, Goll's column, d, Burdach's columns. . . , , . . . 

e and/, mixed lateral paths, k, direct traCtS > (0 the anterior direct pyra- 

cerebeiiar tracts. midal tracts, also called columns 

of Tiirck or uncrossed anterior 
columns. The posterior columns consist of the columns of Goll (at 
the inner side) and the columns of Burdach, which latter have also 
received the name " root zone " (cf. Fig. 146). 

Physiologically, the spinal cord is primarily important as a great 
conducting system, and next as the seat of numerous centres. The 




Fig. 147.— Cross-section through the Spinal Cord at Different Levels, a, 
level of the second. 6, level of the seventh cervical vertebra, c , level of the second, d, 
level of the third lumbar vertebra. (After Quain.) 

motor impulses originate in the brain (cf. pages 172 and 182), and 
travel down along the antero-lateral column chiefly in the crossed 
pyramidal tract of the opposite side, the decussation, as has been 
repeatedly pointed out, taking place for the most part in the medulla 
oblongata. Through the large ganglionic cells of the anterior horns 
these crossed pyramidal tracts are continued into the anterior nerve 
roots and leave as such the spinal cord. The sensory impressions are 



THE REFLEXES. 



419 



transmitted through the posterior roots, hence (some passing through 
the postero-lateral columns) they reach the posterior horns, where 
they at once cross over to the opposite side of the spinal cord. The 
further course of the sensory fibres as they pass to the brain is not 
clearly understood; especially imperfect is our knowledge with re- 
gard to those for the different qualities of sensation — e. g., the sense 
of touch. It seems, however, that the central gray substance must 
be looked upon as the path for impressions of pain (cf. the investiga- 
tions of Edinger about the continuation of the posterior spinal roots 
up to the brain, Anatom. Anzeiger, 1889, iv, 4). 

We know that reflexes originate by the stimulation of a sensory 
nerve. By this an impulse is conducted to a centre, and hence is 
transferred to a motor nerve — reflex arc (Fig. 148). Among such 




Fig. 148. — Reflex Arc. M, motor path. S, sensory path. m, motor (anterior), s, sen- 
sory (posterior) nerve root. 



reflex movements we distinguish (1) skin reflexes caused by irrita- 
tion of the skin, (2) tendon reflexes, which are produced by tapping 
on a tendon. To the former belong the plantar reflex, the centre for 
which is situated in the lower part of the lumbar enlargement, the 
gluteal, the cremasteric, and the abdominal reflexes, which are ob- 
tained by irritating the skin of the buttocks, the inside of the thigh, 
and the abdomen respectively. If we find these present in a patient 
we may assume the centres, which are situated in the lumbar and the 
dorsal cord respectively, to be intact. 

One of the diagnostically most important signs is the condition 
of the so-called patellar reflex. When the tendon of the quadriceps 



420 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



femoris is tapped, a reflex contraction of this muscle ensues by 
which the leg is jerked forward with more or less vigor. This is 
found in most healthy persons. It has been called by Erb " patellar 
tendon reflex " ; by Westphal, who doubted its reflex nature, " knee 
phenomenon "; by Gowers, "knee jerk." 

To a certain extent the mode of tapping this tendon and the 
position of the patient is a matter of indifference. The only points 
to remember are these : The lower leg should be held perfectly loose 
and no superfluous clothing should prevent the proper striking of 
the tendon. The simplest way is to place the patient on the edge of 
a table, remove all clothing from his legs, then, while conversing 
with him about indifferent matters so as to distract his attention 
from what is going on, to observe the effect of the percussion of the 
patellar tendon. 

If we find the reflex present, we may at once conclude that the 
spinal cord at a certain place — that is, from the second to the fourth 
lumbar or first sacral nerves, according to Westphal — is intact. 

If, on the other hand, the reflex is not obtained on the first and 
after repeated examinations, the patient ought to be directed to in- 
terlock his bent fingers and pull strongly (Jendrassik), and only if 
the knee jerk does not occur after repeated trials in the way de- 
scribed should we assume its absence (Jendrassik, Neurol. Central- 
blatt, 1885, 18). It has for some time been Jendrassik's experience 
that the tendon reflexes, more particularly the patellar reflex, is 
much enforced if the other muscles of the body are put into strong 
action (Deutsch. Arch. f. klin. Med., xxxiii). This method of Jen- 
drassik is an excellent and indispensable means in doubtful cases for 
establishing the presence or absence of the knee jerk. 

Besides the patellar reflex, the Achilles tendon reflex, and the 
ankle clonus, the foot phenomenon of Westphal, must be mentioned. 
The latter consists of a succession of clonic contractions of the 
tendo Achillis which occur on a sharp dorsal flexion of the foot. To 
the violent shaking movements of the whole leg, which occasionally 
occur under these conditions, the very inappropriate name of spinal 
epilepsy has been given. 

If the reflex excitability is much increased, a simple tapping on 
the front of the lower leg is sufficient to produce a contraction of 
the calf muscles. This is what the English writers call the " front 
tap." 

Whether all these so-called tendon reflexes are really of reflex 
nature, or whether they are not rather phenomena due to a direct 
stimulation of the muscles (Westphal), is still an unsettled ques- 
tion. 

The same uncertainty exists about a symptom which has by West- 



LOCALIZATION OF SPINAL CORD LESIONS. 



421 



phal been termed " paradoxical contraction," and which consists in a 
muscle remaining in tetanic contraction for quite a time after it has 
been passively shortened. For instance, if we flex the foot of a 
patient lying in bed, the tibialis anticus may under certain conditions 
remain for some time in a state of contraction ; its tendon becomes 
prominent, and only gradually relaxes and allows the foot to return 
to its normal position of rest. Only rarely has this phenomenon 
been observed in other muscles. 

Further reflex centres are found in the lumbar region of the 
spinal cord for the emptying of the bladder and rectum, for the erec- 
tion of the penis and the ejaculation of the semen — reflexes which are 
concerned with the sexual functions. The mechanism of these pro- 
cesses is physiologically by no means understood. Finally, we have 
vaso-motor centres in the cord, of which sufficient mention was, how- 
ever, made on page 394. 

With regard to the localization of the spinal cord lesion, 
two questions arise : (1) Which portion of the cord is dis- 
eased ? Is it the cervical, dorsal, or lumbar? (2) Which part 
of the cross section of the cord ? Is it the gray or the white 
matter or both ? The first question can be answered without 
difficulty in cases where the vertebral column is diseased ; we 
only need to examine the latter by pressing upon the vertebras 
or by applying a hot sponge, etc., over them. Those spots at 
which tenderness is elicited by the application are the seat of 
the disease. The occurrence of spontaneous pain is rarer in 
diseases of the cord. It should, above all, be remembered that 
lesions of the spinal cord, as such, wherever they may be, 
almost never produce pain in the back, but that this is in a 
majority of cases due to trouble in the muscles or their nerves. 
It is a characteristic feature of these pains that they become 
especially marked after prolonged standing and stooping, and 
that they are very bad on rising in the morning. They may 
occur sometimes after a quick movement, in which case some 
muscle bundles have been overstretched or even torn. Pains 
in the back which persist for months and years unaffected by 
any therapeutic measures justify a suspicion of the existence 
of an aortic aneurism which may be pressing against the verte- 
bral column or of enlarged carcinomatous abdominal glands 
(Johnson, British Medical Journal, February 12, 1881). In dis- 
ease of the vertebral column, especially if it be cancerous, pain 
in the back is a prominent symptom, as we have said. 

But, leaving out the tenderness on pressure, there are other 



422 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



symptoms which may help us to decide what segment of the 
cord is diseased in a given case. 

Diseases of the cervical cord generally produce symptoms 
of motor or sensory irritation or of paralysis in the upper ex- 
tremities, pains, paresthesias, feelings of weakness, jerkings, 
and the like in arms, hands, and fingers, to which may be 
added also trophic disturbances. Muscular atrophies and loss 
of reflexes in the upper extremities are often observed. The 
lower extremities, however, remain intact, and the patellar re- 
flex is present and sometimes increased. Repeatedly a very 
decided slowing of the pulse (as low as thirty-two beats to the 
minute in a case of Lebrun, Bull, de l'Acad. de med. de Bel- 
gique, i, 1887, 1) has been met with in lesions of the cervical 
cord and has been attributed to a chronic state of irritation of 
the vagus due to compression or some similar influence. 

Affections of the dorsal cord are mostly accompanied by 
sensory disturbances, paraesthesias in the back, intercostal neu- 
ralgias, aching, boring pains, which sometimes radiate into the 
lower extremities. Anaesthesias, though they are not the rule, 
may be found. If a distinctly circumscribed zone of anaes- 
thesia is made out, it corresponds exactly to the place where 
the lesion in the spinal cord is situated (cf. what will be said 
about lesions of one half of the cord on page 450). 

Lesions of the lumbar cord entail symptoms in the lower 
extremities, giving rise to weakness and paralysis, sometimes 
also jerkings and stiffness; furthermore, to pains, numbness, 
anaesthesias of the legs and feet. The reflexes are lost and 
vesical and rectal symptoms are present, the former consisting 
of retention or dribbling of the urine, pains, strangury, etc. Of 
course, the symptoms may greatly vary according as the whole 
transverse section or only some or even one system of fibres 
alone is affected in the given level of the cord. 

An answer to the second question demands a thorough ac- 
quaintance with the symptoms produced by lesions of the dif- 
ferent portions of the cross section. These we will, therefore, 
now consider. 

I. LESIONS OF THE GRAY MATTER— " POLIOMYELITIS." 

In giving the name poliomyelitis (7roX/o9, gray) to all spinal 
affections confined to the gray matter, we must at once insist 
that these lesions are almost entirely limited to the anterior 
portion of the gray matter, the anterior horns, and more espe- 



LESIONS OF THE GRA Y MA TTER. 



423 



cially to the large ganglionic cells in them. Other portions 
have only rarely been found affected, and then only in connec- 
tion with the just-mentioned lesion. The diseases of the gray 
substance proper which have come under observation were 
confined to the groups of ganglionic cells of which we have 
just spoken. Clinically, there are two such diseases to be dis- 
tinguished, namely, poliomyelitis anterior acuta, or spinal pa- 
ralysis of children (infantile spinal paralysis), and progressive 
muscular atrophy. 



CHAPTER I. 

POLIOMYELITIS ANTERIOR ACUTA — INFANTILE SPINAL PARALYSIS. 

Infantile paralysis, first accurately described by Jacob von 
Heine in 1840, is one of the best-known diseases of the spinal 
cord, both as regards its anatomical seat and its clinical course. 
As has been demonstrated beyond doubt by Charcot, Prevost, 
and Joffroy, it is an acute inflammation of the anterior horns, 
or rather, as is usually the case, of one of them. This leads to 
an atrophy and sclerosis, so that a dense tissue remains, con- 
taining the dilated vessels and small remains of ganglionic cells, 
which are not rarely found to be calcified (Friedlander, cf. 
Fig. 149). The seat of the process is usually either in the 




Fig. 149.— Transverse Section from the Cervical Portion of the Spinal Cord. 
Atrophy and sclerosis of the right anterior horn. (After Charcot.) 

cervical or the lumbar enlargement. In the former case the 
paralysis affects the upper, in the latter the lower extremity. 
The secondary degeneration, which ensues as a consequence of 
the atrophy of the ganglionic cells, extends to the anterior 



INFANTILE SPINAL PARALYSIS. 



425 



nerve roots, the motor nerves, and the muscles supplied by 
them. It is a genuine degenerative atrophy, just as much 
as the one described as coming on after peripheral paral- 
yses. 

Symptoms. — The clinical picture of the disease is very char- 
acteristic. The onset bears a striking resemblance to that of 
cerebral infantile paralysis described on page 271. In the 
midst of perfect health the child is suddenly seized with head- 
ache, vague pains in the limbs, and fever, the temperature 
reaching 104 F. or even more. He becomes stupid and som- 
nolent, and soon, while complete unconsciousness is developed, 
general convulsions set in, which last usually from one to three 
days and then disappear. The patient's condition becomes 
better, consciousness is fully regained, he becomes bright and 
talkative, and the relations think that the malady has already 
spent itself, when unfortunately a more careful examination re- 
veals that the movements of the child are impaired, that one, 
more rarely both, upper or lower extremities are paralyzed. 
The paralysis, which usually affects one arm or one leg, has 
developed rapidly and reached a considerable extent, which, 
however, we would remark, is rarely ever maintained. On the 
contrary, as a rule, it partially recedes and confines itself to 
certain muscles, which then remain permanently paralyzed. 
According to Beevor (cf. lit.), the affection sometimes embraces 
groups of muscles corresponding to those which Ferrier in his 
experiments on monkeys saw contract after stimulation of the 
different cervical nerve roots. In the majority of cases the 
paralysis takes in one leg. The paralyzed muscles rapidly 
atrophy and the electrical excitability undergoes quantitative 
as well as qualitative changes — reaction of degeneration. The 
whole extremity is stunted in its growth, and even the bones 
may be found several centimetres shorter than those of the 
other leg. The appearance of such an extremity in which at 
first all passive motions are possible is quite characteristic. 
The skin is pale, cyanotic, and feels cold, but retains its sensi- 
bility completely. Skin and tendon reflexes are lost, but there 
are no vesical symptoms. Later on secondary contractures 
develop, among which the so-called "paralytic clubfoot" is the 
best known. In consequence of the paralysis of the peroneal 
muscles, their antagonists, the calf muscles, become perma- 
nently contracted and cause the point of the foot to hang 
down. In the arms analogous conditions may be found, the 



426 DISEASES OF SUBSTANCE OF SPINAL CORD. 

non-paralyzed antagonists always assisting in the production 
of the contractures. 

Roughly speaking, this is the course in most cases, only oc- 
casionally the initial fever may be slight enough to be over- 
looked and the paralysis develop without the child ever having 
taken to his bed. In rare cases the convulsions, instead of last- 
ing days, continue for weeks. In others, again, several months 
may pass before the onset of the actual paralysis ; but all these 
are the exceptions which need not confuse us in making a diag- 
nosis. The further general development (with the exception 
of that of the paralyzed extremity) is perfectly normal, and 
neither, as happens in the cerebral infantile paralysis, does the 
mind become in any way impaired nor do the initial convul- 
sions ever recur. The child grows up in good health, but al- 
ways remains, especially if one leg is affected, a cripple. If, as 
often happens, contractures or a spontaneous paralytic luxation 
of the hip develop, the patient has for years to be under the 
care of the surgeon and needs braces and the like. If an 
arm is affected, the capability of the patient for making 
his living is naturally considerably and permanently inter- 
fered with. 

Diagnosis. — It is not difficult to avoid mistaking the disease 
for any other if we bear in mind the characteristic onset, the 
localization, the behavior of the paralysis itself, the flaccid con- 
dition of the muscles, the absence of the reflexes, and the cold 
and cyanotic skin. Where we find a hemiplegia — i. e., where 
the arm and leg of the same side are paralyzed — we should in 
children always first think of infantile spastic hemiplegia (page 
272), as it is one of the rarest exceptions for the spinal paraly- 
sis to take on this distribution. Confusion with the syphilitic 
pseudo-paralysis, also known under the name of Parrot's dis- 
ease, is avoided by remembering the fact that in this disease 
the paralysis makes its appearance immediately or at least with- 
in a few days after birth (Dreyfouss, Revue de med., aout 1885, 
v), while Heine's paralysis of children does not occur at such 
an early age. 

Prognosis. — The prognosis, as soon as the initial acute 
symptoms have passed, is, as far as life is concerned, absolutely 
favorable ; as far as the recovery of function in the affected ex- 
tremity is concerned, equally unfavorable. Any notable im- 
provement is very rare, complete cure out of the question. 
These points should be carefully considered before inducing a 



INFANTILE SPINAL PARALYSIS. 



427 



poor and struggling father to let his child undergo year after 
year an expensive and useless course of treatment. 

^Etiology. — Of the aetiology of the disease we know noth- 
ing. It is doubtful whether cold is ever a causative factor. It 
is possible that infectious influences, the action of certain micro- 
organisms, will at some time be proved to be the cause of the 
disease. For the present, however, this is nothing more than 
a hypothesis which has not gained any firmer ground from the 
report of Cordier of an epidemic of the disease (Lyon med., 
1888, 1, 2). In a small village thirteen children were inside of 
two months taken ill with anterior poliomyelitis and four died. 
According to Cordier, the appearance of the disease in sum- 
mer, the sudden onset, the similarity in course, speak for an 
infectious origin, the infection, as he supposes, taking place 
through the air passages. 

Treatment. — Little more is known about the treatment than 
about the aetiology. All measures to cure or even merely to 
improve this rapidly developed paralysis are more or less use- 
less. Electrical treatment with the faradic or galvanic current, 
systematic massage, gymnastic exercises, together with rubbing 
with all sorts of salves — all these have been tried without any 
noteworthy success. In a few cases I have seen the method- 
ical use of heat, in the form of hot sand baths, warm packs, etc., 
bring about at least a perceptible improvement ; but even here 
this was out of proportion to the care and trouble which had 
been taken. Certain it is that the influence of the different 
baths has been greatly overrated, whether it be the brine 
baths of Kreuznach, Reichenhall, Kolberg, or the chalybeate 
springs of Pyrmont, Flinsberg, Schwalbach, or the sodium 
waters of Rehme, Soden, or finally the non-medicated hot 
springs of Gastein, Johannisbad, and many others, each of 
which has its advocates. The most appropriate appear to be 
those last mentioned, but in most cases we shall even then find 
that while perhaps the child's general condition is improved 
and it becomes strong owing to the good hygiene and fresh 
air, the paralysis, for the sake of which all has been undertaken, 
remains absolutely unchanged and presents no improvement. 

In view of these unsatisfactory results, the interesting but 
still scanty communications, according to which the growth 
of bone can artificially be increased, deserve our deep interest. 
In 1887 Helferich proposed to tie round the affected (paralyzed, 
atrophic) limb elastic rubber tubing so as to produce an arti- 



428 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



ficial engorgement, and through this a more active nutrition 
of all the tissues, including the bones. Schuller also has re- 
ported before the Berlin Medical Society, November 28, 1888 
(Deutsch. Med.-Ztg., 1888, 99, page 1182), several cases which 
were thus treated and which showed decided improvement. 
To judge from his communication, this treatment undoubtedly 
should be tried in all suitable cases. It is, however, a proced- 
ure which, as well as the orthopaedic treatment so important 
for the prevention of deformities, should not be undertaken 
without consulting a surgeon. 

LITERATURE. 

Prevost. Compt. rend, de la Soc. de biol., 1866, p. 215. 

Charcot et Joffroy. Arch, de physiol., 1870, v, p. 135. 

Roger et Damaschino. Gaz. med., 1 871, 41, 43. 

Charcot. Lectures on the Diseases of the Nervous System, delivered at La 

Salpetriere. Translated by George Sigerson. New Sydenham Society, 

London, 1877. 
Friedlander, C. Ueber Verkalkung der Ganglienzellen. Virchow's Archiv, 

1882, 88, 1. 
Rockwitz. Deutsche Zeitschr. f. Chir., 1883, xix, 2, 3. 
Sahli. Deutsches Archiv f. klin. Med., 1883, xxxiii, 3, 4. 
Beevor. Med.-Chir. Transact., 1885, lxviii, p. 205. 
Philips. Brit. Med. Journ., July 10, 1886. 
Lorenz. Ueber die Entstehung der Gelenkscontracturen nach spinaler Kinder- 

lahmung. Wiener med. Wochenschr., 1887, 27-31. 
Karewski. Die der spinalen Kinderlahmung folgenden Gelenkscontracturen und 

die paralytische Luxation der Hiifte. Archiv f. klin. Chir., 1888, 37, 2, p. 346. 
Cordier. Lyon m6d., 1888, lvii, 1, 2. 
Rieder, Hermann. Poliomyelitis ant. acuta. Miinchener med. Wochenschr., 

1889, xxxvi, 2. 

Though the lesions of the gray anterior horns when occur- 
ring in children are well understood, both in their anatomical 
and their clinical aspect, yet when the same process takes place 
in adults our knowledge becomes very limited. Here the ma- 
terial at our disposal is still so small that only in rare excep- 
tions can we say definitely whether we are dealing really with 
an anterior poliomyelitis and not rather with a peripheral dis- 
ease, a multiple neuritis. Clinically, the differential diagnosis 
between the two can only be made in the initial stage, as the 
peripheral disease is accompanied with pains and sensory dis- 
turbances which are absent in the central affection. 

A patient is taken ill with grave general disturbances — 



CHRONIC ANTERIOR POLIOMYELITIS. 



429 



fever, somnolence, convulsions, delirium, etc. — and within a 
short time, perhaps in one or two weeks, a widespread paraly- 
sis in all four extremities is developed. The paralyzed mus- 
cles become flaccid and atrophy, the tendon reflexes disappear ; 
sensation, however, as well as bladder and sexual functions, 
present no abnormity. With a history like this we must think 
of a lesion of the anterior gray horns. This idea becomes more 
than a conjecture if on examination the affected muscles are 
found to be such as are supplied from ganglionic cells, which 
most probably lie in close proximity to one another in the 
spinal cord. In such cases, as Remak has shown so beautiful- 
ly, certain types of paralysis are observed — the forearm type 
(paralysis of all the extensors without the supinator longus) 
and the upper-arm type (paralysis of the biceps brachialis an- 
ticus, deltoid, and the supinator longus) — but unfortunately 
such instances are rare, and therefore even quite an experi- 
enced physician may feel uncertain about the diagnosis. 

The difficulty becomes greater if the paresis or paralysis is 
not extensive and does not develop rapidly, but slowly and by 
fits and starts. In these cases not rarely a temporary improve- 
ment may be noted and arouse hopes of complete recovery, 
unfortunately never justified. These are the instances in which 
we find not complete, but partial reaction of degeneration in 
the paralyzed muscles — intermediate form of chronic anterior 
poliomyelitis (Erb). It goes without saying that we must have 
the other symptoms, especially the loss of reflexes, even to jus- 
tify a conjectural diagnosis. Moreover, it is necessary that 
there should be absolutely no sensory changes and that blad- 
der and sexual functions should be normal. Of the points of 
difference between anterior poliomyelitis and tabes we shall 
speak later. 

We can hardly expect much from any treatment. Elec- 
tricity, however, should be tried, if for no other reason than 
that something is done. Duckworth recommended, besides, 
belladonna, iron, quinine, and cod-liver oil, and claims to have 
cured cases with these remedies. 

With reference to the aetiology, nothing certain is known. 
Whether traumatism can ever cause anterior poliomyelitis re- 
mains doubtful, notwithstanding the report of Gibbons (Med. 
Times and Gazette, September 5, 1885). He had among his 
patients a boy nine years of age who after a fall on his knees 
developed the symptoms of an anterior poliomyelitis (and re- 



43© 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



covered completely !). In cases of chronic anterior poliomye- 
litis which came to autopsy, sometimes atrophy in the gangli- 
onic cells of the anterior horns through the whole length of 
the cord, as well as atrophy of the anterior roots, was observed, 
while the peripheral nerves remained intact (Oppenheim). 

LITERATURE. 

Lelvir. Progr. med., 1881, ix, 42, 43. 

Erb. Ueber das Vorkommen der chron.-atroph. Spinallahmung beim Kinde. 

Neurol. Centralbl., 1883, ii, 8. 
Bernhardt. Virchow's Archiv, 1883, Bd. 92, p. 369. 
Duckworth. Clinical Lecture on Subacute Anterior Spinal Paralysis (Ant. 

Cornual Myelitis) in the Adult. Lancet, November 14, 1885. 
Leclers et Blanc. Paralysie spinale de l'adulte. Lyon med., 1886, 52. 
Buss. Ein seltener Fall von atrophischer Spinallahmung (Poliom. ant. chron. 

adult.) mit Uebergang in acute Bulbarmyelitis. Berliner klin. Wochenschr., 

1887, No. 28. 
Oppenheim. Ueber Poliomyelitis ant. chron. Deutsche Med.-Ztg., 1887, 95, p. 

1087. 
Oppenheim. Archiv f. Psych, u. Nervenkrankheiten, 1888, xix, 2, p. 381. 



CHAPTER II. 

ATROPHIA MUSCULARIS PROGRESSIVA SPINALIS — PROGRESSIVE 
MUSCULAR ATROPHY. 

Progressive muscular atrophy was first described by Du- 
chenne and Aran in 1849 an d 1850, and was recognized by 
Cruveilhier in 1855 as a spinal affection. Thanks to the work 
of Lockhart-Clarke, and especially that of Charcot, the occur- 
rence of a pathological process restricted to the gray substance 
of the spinal cord, which is accompanied by a muscular atrophy 
of typical distribution, is now established beyond the slightest 
doubt. 

Pathological Anatomy. — The process, which is usually most 
pronounced in the cervical cord, consists again of an atrophy 
and transformation of the gray anterior horns into a fine fibrous 
tissue containing spider cells. The large ganglionic cells are 
partly or wholly destroyed, or at any rate are diminished in 
number and perceptibly smaller. Here, too, the lesion extends 
to the anterior nerve roots and the corresponding fibres of the 
motor nerves. On microscopical examination we find that the 
muscles supplied by them retain their transverse striation, but 
the fibres are decidedly diminished in size. Some fibres also 
show the so-called degenerative atrophy — that is, a fatty, wax- 
like degeneration, with increase of the interstitial connective 
tissue and multiplication of the muscle nuclei. Which of the 
described processes has to be regarded as the primary one, 
or, in other words, whether the disease actually does start in 
the gray matter of the cord and not perhaps in the peripheral 
nerve endings, or whether this differs in different cases, we 
are unable at present to decide. One thing we ought to keep 
in mind with reference to the anatomical seat of the affection, 
namely, that in the cord no other parts than the ones men- 
tioned are affected, and more especially that the pyramidal 
tracts always remain intact. 



432 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



Symptoms. — The onset of the disease is in many cases very 
characteristic. The patient begins to complain of weakness in 
the arms, sometimes more in the right than in the left, which 
soon interferes to some extent with his ordinary actions. Sen- 
sory changes and pains are absent, a point which is of vast 
diagnostic importance. Not many weeks after these symptoms 
have appeared the competent observer will notice a peculiar 
flatness, a sunken-in condition of the ball of the thumb, while at 
the same time the thumb is more than usually approximated to 
the second metacarpal bone ("ape hand," Fig. 150). The in- 





Fig. 150. Fig. 151. 

Figs. 150, 151. — Progressive Muscular Atrophy. (After Eichhorst.) Fig. 150. Ape- 
hand. Fig. 151. Sunken-in interosseal spaces on the back of the hand. 

terosseal spaces on the back of the hand are sunken in and the 
terminal phalanges of the fingers are in incomplete extension 
(Fig. 151). The hollow of the hand seems flattened (atrophy 
of the lumbricales) and the atrophy of the muscles of the the- 
nar and hypothenar becomes more and more apparent. As 
the function of the interossei becomes disturbed to a greater 
extent, the same claw-like position of the fingers develops 
which has been described on page 349 as occurring in affec- 
tions of the ulnar nerve (" claw hand," "main en griffe"). 

After this condition has thus for weeks or months under- 
gone no marked change, the disease begins to attack either the 
muscles of the forearm, or, passing over these, implicates the 
muscles of the shoulders and with special preference the del- 
toid. In the former case the extensors are attacked earlier and 
more seriously than the flexors. The muscles of the trunk and 



PROGRESSIVE MUSCULAR ATROPHY. 433 

legs are either later or never affected, but if the diaphragm 
and other respiratory muscles are invaded this may prove 
fatal as well as an extension of the process from the cord to 
the medulla oblongata, in which case the symptoms of pro- 
gressive bulbar paralysis are superadded (page 154). If this 
does not take place and the respiratory muscles are spared, 
the disease may last for years and tens of years and death is 
only caused by an intercurrent acute malady. 

Apart from the characteristic onset, the following signs 
help to make the diagnosis certain: (1) Fibrillary twitchings in 
the affected muscles, which can at times be produced by tap- 
ping the muscles, but which often are seen to appear of their 
own accord and continue without interruption. (2) The condi- 
tion of the electrical excitability, which depends directly on 
the number of muscle fibres left. If the greater number of 
the fibres are wasted, then the excitability for both currents is 
equally decreased. If all the fibres of a muscle have disap- 
peared and only fat and connective tissue remain, the excita- 
bility of the muscle is completely lost. It is only exceptionally 
that the excitability also undergoes qualitative changes and we 
find reaction of degeneration. (3) The loss of the tendon re- 
flexes, which is sufficiently explained by the disappearance of 
the ganglionic cells, a part of the reflex arc. It is only because 
the lower extremities are rarely affected that the patellar re- 
flexes are usually retained. (4) Sensibility remains everywhere 
and for any kind of impressions intact (touch, pressure, pain, 
temperature). The coldness and blueness of the hands is to be 
attributed to the disuse of the muscles. True trophic disturb- 
ances of the skin, as well as bladder and rectal symptoms, are 
usually absent. 

Diagnosis, — Remembering, then, the different points just al- 
luded to, the diagnosis should be easy, and it will not be diffi- 
cult to avoid confounding the disease with myelids, neuritis, or 
syringomyelia. The flaccid paralysis, the absence of all symp- 
toms of motor irritation and sensory disturbances, is especially 
of moment in differentiating this disease from myelitis. More 
particularly characteristic is the commencement, the onset of 
the disease in the small muscles of the hands. If this has been 
well pronounced an error in diagnosis is unpardonable. 

Etiology . — With reference to the aetiology a little more is 
known about this disease than about spinal infantile paralysis ; 
for certain cases at least it has been shown that overexertion 
28 



4 34 DISEASES OF SUBSTANCE OF SPINAL CORD. 

of the muscles, as happens sometimes to those who work with 
the sewing machine, has a causative influence, or at any rate 
the disease has been preceded by some overexertion of the 
muscles, to which we are then justified in attributing an aetio- 
logical importance. The conditions, however, under which 
paralysis and fatigue of the muscles lead to atrophy — why, for 
instance, the serratus magnus (Chvostek) is in some cases at 
first thus affected — we are wholly ignorant of, just as we do not 
know the conditions under which the genuine hypertrophy de- 
velops which we often find in the biceps of blacksmiths. Re- 
cently Bernhardt has again drawn attention to the fact that 
the disease may be hereditary (Virchow's Archiv, 1889, 115, 2). 
Little need be said about the therapeutics ; there is no 
effectual treatment, and all measures that have been tried have 
not been efficient in hindering the progress of the disease. 

LITERATURE. 
(Cf. also pages 414 and 415.) 
Chvostek. Oesterr. Zeitschr. f. prakt. Heilk., 1871, xvii, 13-16. 
Lockhart-Clarke. Med.-Chir. Transact., 1873, Ivi, p. 103. 
Charcot. Lectures on the Diseases of the Nervous System, delivered at the 

Salpetriere. Translated by George Sigerson. New Sydenham Society, 

London, 1877. 
Pierret et Troisier. Arch, de physiol., 1875, 2me s & r -> "\ 2. 
Bode. Casuist. Beitrage zur /Etiologie, Symptome und Diagnose der progress. 

Muskelatrophie. Inaug. Diss. Halle, 1881. 
Westphal. Charite-Annalen, 1886, xi, p. 357. (Progressive muscular atrophy, 

with implication of the facial muscles.) 
Schultze, F. Ueber den mit Hypertrophic verbundenen progressiven Muskel- 

schwund und ahnliche Krankheitsformen. Wiesbaden: Bergmann, 1886. 
Landouzy et Dejerine. Nouvelles recherches cliniques et anatomo-pathologiques 

sur la myopathie atrophique progressive a propos de six observations nou- 
velles dont une avec autopsie. Revue de med., 1886, vi, 12, 977-1027. 
Charcot et Marie. Sur une forme particuliere d'atrophie musculaire progressive, 

etc. Ibid., 1886, vi, 2, p. 97. 
Ladame. Contribution a l 1 etude de la myopathie atrophique progressive. Ibid., 

1886, vi, 10, p. 817. 
Striimpell, A. Deutsches Arch. f. klin. Med., 1887, Bd. xlii, 1-3, p. 230. 
Bernhardt. Ueber einen Fall von (juveniler) progressiver Muskelatrophie mit 

Betheiligung der Gesichtsmusculatur. Berliner klin. Wochenschr., 1887, 

No. 41. 
Spillmann et Haushalter. Observation de myopathie progressive primitive a 

type facio-scapulo-humerale. Revue de med., 1888, vi. 
Sachs. Progressive Muscular Dystrophies ; the Relation of the Primary Forms 

to one another and to Typical Progressive Muscular Atrophy. Journ. of 

Nerv. and Ment. Dis., 1888, xiii, 11. 



PRIMARY LESIONS OF THE WHITE COLUMNS. 435 



II. LESIONS OF THE WHITE MATTER OF THE SPINAL CORD— 
" LEUCOMYELITIS." 

While, as we have said on page 422, the lesions affecting 
the gray matter (poliomyelitis) are almost entirely confined to 
one portion of it — namely, the anterior horns — we shall soon 
see that this is different with the lesions of the white matter, 
to which the general name leucomyelitis may be given (Xeiz/co?, 
white). Here different parts can be attacked, either alone or 
in conjunction with others, and it is of great importance to 
differentiate between the clinical symptoms which occur in 
the diseases of the different columns or " systems " (Flechsig), 
hence called " system diseases." 

The affection is either a primary one, when it is often im- 
possible to ascertain any aetiological factor, or it occurs sec- 
ondarily and as a consequence of certain affections of the 
brain (cf. page 229) and the spinal cord itself, such as trau- 
matic inflammations and compression. We shall consider both 
separately. 

A. Primary Lesions of the White Columns. 

Regarded from an anatomical standpoint, the primary tract- 
degenerations of the white substance consist in a destruction of 
the nerve fibres and a simultaneous increase of the neuroglia. 
The medullary sheaths are the first to disappear; the axis cylin- 
ders, which are more resistant, do not degenerate till later. 
Compound granular corpuscles, which remove the detritus 
from the diseased regions (Ziegler), accumulate in the lymph 
sheaths of the vessels. The increasing neuroglia crowds in 
and displaces the empty nerve tubes, a process which, in con- 
junction with the thickening of the walls of the vessels, which 
develops at the same time, is described under the name of scle- 
rosis, or gray degeneration. 

An affection confined to one nerve tract or system has up 
to this time only been observed in the antero-lateral, but not in 
the posterior columns. In the former, the anatomical arrange- 
ment of which has been described on page 418, we meet espe- 
cially frequently with sclerosis of the so-called crossed pyram- 
idal tracts, but the lesion does not necessarily extend over 
the whole length of the tract, but may be only partial (West- 
phal). Most of the cases which have come under observation 



436 DISEASES OF SUBSTANCE OF SPINAL CORD. 

were, however, not pure instances, but presented other ana- 
tomical changes as well, and there is only one case reported, 
by Dreschfeld, in 1881, which, viewed from an anatomical 
standpoint, can pass for a pure lateral sclerosis. 

The primary sclerosis of the lateral columns — spastic spinal 
paralysis, tabes dorsale spasmodique—was, first described by Erb 
and Charcot in 1875, and characterized by them as a motor 
paralysis with remarkable increase in the tendon reflexes; and, 
indeed, if we examine such patients, all we find is that they 
have lost to a greater or lesser extent the use of their legs ; 
they are unable to walk, the feet are glued, as it were, to the 
floor, and the patient can only shuffle along, the inner margin 
of the foot never leaving the ground. At the same time the 
muscles feel firm and hard, the legs are in extension, and any 
attempt at flexion is difficult. If such a patient is made to sit 
on the edge of a table the legs do not hang down flaccidly, as 
might be expected, but are thrown into a state of tetanic 
tremor, produced by contractions of the quadriceps extensor. 
There is an enormous exaggeration of the patellar reflexes, and 
the ankle clonus is obtained without the slightest difficulty. 
With the exception of the inability to walk, the patient has no 
subjective complaints ; neither sensation nor the functions of 
the bladder, rectum, or the sexual apparatus show any abnor- 
mity. An implication of but one of these would at once 
exclude the diagnosis of lateral sclerosis, as would also (and 
this should be especially remembered) the existence of any 
muscular atrophy. The very characteristic spastic or spastic- 
paretic walk of the patient, the traces which his feet leave on 
a gravel path, for instance, and which can be followed up as 
distinct continuous streaks, the shuffling noise which accom- 
panies every step when he attempts to walk about the room, 
these are of great diagnostic value ; the examination of the 
soles of the patient's shoes, which appear thinner and more 
worn down on the inner side, will be of interest and value. 

The disease begins in youth or in middle life, attacking 
first the one then the other leg, without, as a rule, extending to 
the arms or trunk, yet the upper extremities are said to be 
occasionally affected (Striimpell). The disease may last years 
or tens of years without presenting any decided change for the 
worse. Death is brought about by intercurrent diseases. It 
is not known whether, as in progressive muscular atrophy, 
overexertion is of astiological importance ; instances, however, 



FRIEDREICH'S DISEASE. 437 

where acrobats (Donkin) and hod-carriers (Munter) were at- 
tacked seem to suggest this. Morgan pointed out that ex- 
posure to cold, such as long standing in water, may be the 
immediate cause of the disease (Lancet, January 19, 188 1). 

Much more frequent than a lesion confined to the crossed 
pyramidal tracts is one which implicates not only these, but 
with them the posterior columns and the direct cerebellar 
tracts, in which, although not always, Clarke's columns take 
part. The anatomical character of this " combined system 
disease " which results from these lesions has been repeatedly 
described (Westphal, Gowers, Striimpell). The symptoms 
vary according to the distribution of the lesion ; thus, if the 
disease of the lateral columns extends low down, while the 
posterior columns in the dorsal and lumbar region present no 
changes, rigidity of the muscles and increase of the reflexes 
will be found. If, on the other hand, the disease in the poste- 
rior columns extends further downward, these symptoms will 
be absent, the lesion in the lateral being neutralized as it were 
by that in the posterior columns (Westphal). 

Not rarely the affection seems to depend on faulty develop- 
ment, a condition which we may meet with in more than one 
member of the same family, and which may be hereditary. In 
these cases the disease appears in early childhood, and, as we 
said, sometimes in several children of the same family. It has 
been called, after the author who first described it, Friedreich's 
" hereditary ataxia." The motor disturbances in the children 
begin in the feet, the walk becomes awkward, they stumble, 
and in passing over small obstacles have to look at their feet to 
keep from falling, etc. The patellar reflexes disappear ; the 
arms are not affected until later, and, indeed, they are by no 
means always implicated. The second motor disturbance es- 
tablishes itself in the muscles of the tongue and the lips which 
are necessary for speaking, and this produces a very charac- 
teristic defect of speech of motor origin. Finally, the muscles 
of the eyes become implicated, and there results a distinct 
nystagmus. The combination of these three symptoms is 
pathognomonic for this rare disease. It has no connection 
with tabes and sensory changes, and bladder symptoms, mani- 
festations which are probably never wanting in cases of tabes, 
are never met with in the disease under consideration. Nor 
can it be mistaken for multiple sclerosis, as vertigo and " scan- 



438 DISEASES OF SUBSTANCE OF SPINAL CORD. 

ning speech " are never associated with it. The course is 
tedious, the prognosis always unfavorable, the muscles under- 
go atrophy in consequence of inactivity, and contractures oc- 
cur in the joints. 

Similar symptoms are observed in adults in cases of com- 
bined lateral and posterior sclerosis ; yet there are certain 
peculiarities to which Gowers especially has drawn attention. 
The disease was named by him " ataxic paraplegia." The 
lower extremities are ataxic and paretic, which gives rise to an 
uncertain, swaying walk ; but this is associated with parsesthe- 
sias, weakness of the sphincters, and decrease of the sexual 
power. The patellar reflexes are at first increased, and only 
at times become lost later in the disease. Such an increase is 
never known in hereditary ataxia. During the period of in- 
crease, rigidity of the muscles, spasm, and ankle clonus are 
present. It is evident that cases of this kind may be mistaken 
for tabes, especially if the patellar reflexes are absent, as excep- 
tionally occurs. Then the history may be of use to us, as 
syphilis seems to possess no ^etiological importance whatever 
in the combined sclerosis, while exposure to cold and over- 
exertion seem to be of considerable moment. 

LITERATURE. 
Spastic Spinal Paralysis. 

Leyden. Archiv f. Psych, und Nervenkrankh., 1878, viii, 2, p. 761. (Experi- 
mentally produced spinal sclerosis.) 

Mobius. Zur spastischen Spinalparalyse. Schmidt's Jahrb., 1880, Bd. clxxxviii, 
p. 129. (Many references.) 

Donkin. Brit. Med. Journ., December 9, 1882. (Spastic paraplegia in an 
acrobat.) 

Westphal. Ueber einen Fall von sog. spastischer Spinalparalyse mit anat. 
Befunde. Archiv f. Psych, und Nervenkrankh., 1884, xv, 1, 224. 

Pitres. Un cas de paralysie generate spinale anterieure subaigue suivi d'autop- 
sie. Progr. med., 1888, 35. 

Knuth. Ueber spastische Spinalparalyse mit Dementia paralytica. Kiel, 1888. 

Richardson. Case of Infantile Spastic Paralysis. Lancet, November, 1888, 
ii, 19. 

Friedreich 's Disease. 

Brousse. De l'ataxie hereditaire. Paris, 1882. (Maladie de Friedreich.) 
Rutimeyer. Virchow's Archiv, 1883, Bd. xci, 2. 
Erlenmeyer. Centralbl. f. Nervenheilk., 1883, vi, 17. 
Walle. Schweizer Corresp.-BL, 1884, xiv, 2. 
Musso. Riv. clin., 1884, xxiii, 10. 



SECONDARY LESIONS OF THE WHITE COLUMNS. 439 

Longuet. L'Union, 1884, 72. 

Schulze, F. Arch. f. Psych, und Nervenkrankh., 1884, xv, 1, p. 262. 

Seguin. New York Med. Record, 1885, xxvii, 29. 

Sinkler. Journ. of Nerv. and Ment. Diseases, 1885, xii, 3. 

Ormerod. Med.-chir. Transact., 1885, lxviii, p. 147. 

Judson, S. Bury. Brain, July, 1886, ix. 

Stintzing. Miinchener med. Wochenschr., 1887, Bd. xxxiv, 21. 

Charcot. Progr. med., 1887, 23. 

Riitimeyer. Ueber hereditare Ataxic Virchow's Arch., 1887, no, 2. 

Ormerod. Brain, 1888, xxxix and xl. 

Gilles de la Tourette. Nouv. iconograph. de la Salpetr., 1888, 3. 

Combined System Diseases. 

Kahler und Pick. Arch. f. Psych, und Nervenkrankh., 1877, viii, p. 251. 

Prevost. Arch, de physiol., 1877, 2me ser., iv, 3, 4, 5. (Combined sclerosis of 
the posterior and lateral tracts.) 

Striimpell. Archiv f. Psych, und Nervenkrankh., 1880, xi, 1. 

Edes. The Somewhat Frequent Occurrence of Degeneration of the Postero- 
lateral Columns of the Spinal Cord in so-called Spinal Concussion. Boston 
Med. and Surg. Journ., September 21, 1882. 

Grasset. Du tabes combine (ataxo-spasmodique) ou sclerose postero-laterale de 
la moelle. Arch, de neurol., 1886, xi, xii. 

Gowers. Ataxic Paraplegia. Lancet, 1886, ii, 1, 2. 

Babinski et Charrin. Sclerose medullaire systematique combinee. Revue de 
med., 1886, iii, 11, p. 962. 

Striimpell. Ueber eine bestimmte Form der primaren combinirten Systemer- 
krankung des Ruckenmarks. Arch. f. Psych, etc., 1886, xvii, 1. 

Erlicki et Rybalkin. Zur Frage iiber die combin. Systemerkrankungen des 
Ruckenmarks. Ibid., 1886, xvii, 3. 

Dana. Progressive Spastic Ataxia (Combined Fascicular Sclerosis) and the 
Combined Sclerosis of the Spinal Cord. The Med. Record, July 2, 1887. 

Adamkiewicz. Wiener med. Wochenschr., 1888, 17. 

Kiewlicz. Arch. f. Psych, und Nervenkrankh., 1889, xx, 1. (Myelitis trans- 
versa, syringomyelia, multiple sclerosis, and secondary degenerations.) 

B. Secondary Lesions of the White Columns. 

Lesions of the motor centres of the brain cortex, or lesions 
of the path between these centres and the motor ganglia of the 
spinal cord, the so-called cortico-muscular tract or pyramidal 
tract, give rise to a descending degeneration of the motor fibres 
on the same side as the brain lesion. This secondary degen- 
eration is in the cord continued in the crossed pyramidal tract 
of the opposite side, while the direct pyramidal tract only pre- 
sents traces of it. About the causes of this sclerosis we possess 
just as little definite knowledge as about the clinical symptoms 
by which it manifests itself. The former is sought in the cut- 
ting off of the parts from their trophic centres, and with regard 



44© 



DISEASES OF SUBSTANCE OF SPINAL CORD. 




to the latter it is generally supposed that the gradual develop. 

ing rigidity of the muscles, the increase of the reflexes, and the 
later contractures depend on this, degener- 
ation. The cases, however, in which at the 
autopsy an extensive de- 
generation was found, 
while during life not a 
trace of such symptoms 
was present, do not 
speak much in favor of 
this view. 

Lesions of the whole 
transverse section of the 
cord also produce sec- 
ondary degeneration, 
which, however, not 
only extends downward 
descending degener- (in the pyramidal tracts), 

ation in the Spinal i - i j / \ • 

r .. n A . but also upward — (i) in 

Cord. A, primary area , r v J 

of degeneration (lesion), the inner segment of the 

2?, degeneration of Goll's posterior Columns (Goll, 
columns (ascending). C, , _,. . , ; . . 

degeneration of the cf - Fl g; J 52), and (2) in 

crossed pyramidal tract the direct cerebellar 

gZ:*T (After tracts (Flechsig), which 
are in connection with 
Clarke's columns (cf. Fig. 153). While 
this ascending degeneration is physio- 
logically extremely interesting, as it in- 
dicates that the trophic centres of these 
two tracts must be situated more pe- 
ripherally (as, for instance, in Clarke's 
columns), we are not as yet able to at- 
tribute any clinical importance to it. 



Fig. 152. — Ascending and 




Fig. 153.— Secondary As- 
cending and Descend- 
ing Degeneration in 
a Transverse Affec- 
tion of the Upper 
Dorsal Cord. The as- 
cending degeneration oc- 
curring in Goll's columns 
and the direct cerebellar 
tracts, the descending de- 
generation in the crossed 
pyramidal tracts. (After 
Strumpell.) 



III. LESIONS OF THE GRAY AND WHITE MATTER OF THE 
SPINAL CORD. 

Charcot and Joffroy were the first to show that the large 
ganglionic cells of the gray anterior horns and the pyramidal 
tracts can be affected simultaneously by a disease which pro- 
duces characteristic clinical symptoms, but it was not until 
Flechsig announced his discovery of the system of conducting 



AMYOTROPHIC LATERAL SCLEROSIS. 



441 



fibres that these clinical observations became fully understood. 
Now we know that the disease which the French authors, fol- 
lowing Charcot, have termed sclerose late'rale-amyotrophique, 
amyotrophic (more properly myo-atrophic) lateral sclerosis, 
consists of a lesion of the cortico-muscular tract which begins 
as a degenerative atrophy in the lumbar cord and which, as 
Charcot and Marie have lately pointed out, can be traced as 
far as the motor ganglionic cells of the central convolutions. 
Attention has already been called to the fact that, just as the 
ganglionic cells of the anterior horns, in the same way the 
motor nuclei of the medulla oblongata may be implicated, and 
thus the clinical picture of progressive bulbar paralysis de- 
velop. The two diseases are therefore analogous, and akin to 
them is a third — namely, the progressive spinal muscular atro- 
phy — in which affection also the large ganglionic cells are dis- 
eased, as we have already pointed out on page 431. From the 
ganglionic cells the atrophy spreads toward the periphery to 
the anterior nerve roots and the muscles supplied by them. 

That the clinical manifestations are strictly motor and 
trophic, and that no sensory changes can occur, we can well 
understand from the anatomical distribution of the lesion. The 
patients at first complain of weakness in the arms and the 
hands, which soon interferes with their occupation. This loss 
of strength increases fairly rapidly, and the atrophy in the 
muscles of the hand — the thenar, the antithenar, and interossei 
—becomes more and more apparent. 

The muscles of the arms also waste, more especially those 
of the extensor side, and the former roundness of the shoulder 
is soon lost owing to the atrophy of the deltoid. The triceps 
and other muscles also then take part in the lesion, and the 
helplessness of the patient, who has but little use of his upper 
extremities, rapidly increases. At the same time the tendon 
reflexes are increased and tapping of the bones of the forearm 
elicits lively contractions of the muscles (" periosteal re- 
flex"). 

That the so-called "jaw-jerk," which has been described by 
De Wattewille, is characteristic of the disease I am very much 
inclined to doubt, since in a number of perfectly healthy per- 
sons I found it in some present, in some absent. It certainly 
does not possess any diagnostic value. This jerk may be pro- 
duced by pressing down the lower jaw by means of a broad 
paper-cutter and tapping the latter with a percussion hammer 



442 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



near the teeth. The lower jaw will then respond with a con- 
traction of the muscles of mastication. 

In a relatively short time the paralysis of the upper ex- 
tremities has become so complete that not even the slightest 
motion is possible, and gradually contractures develop (by 
preference in the wrist and elbow joint). In the lower ex- 
tremities the same changes may be noted, but they make their 
appearance later and do not reach such a high degree. Here, 
too, we have first weakness, difficulty in walking, and general 
awkwardness in making movements, then rigidity and stiffness 
of the muscles, enormously increased patellar reflexes and 
ankle clonus, later on total immobility and contractures in hip, 
knee, and ankle joints. 

A case in one of my wards, a woman thirty-four years of 
age, has been for two years without power of motion, and is so 
entirely deprived of the use of her four extremities that with- 
out assistance she is unable to make even the slightest motion 
with either fingers, hands, arms, toes, feet, or legs. The dis- 
ease goes on to invade the motor nuclei of the medulla ob- 
longata, and hence is produced difficulty in swallowing, which 
ultimately amounts to a total inability to get food down, and 
the patient dies of starvation. At other times a disturbance of 
the respiratory apparatus may bring about a fatal issue. It is 
exceptional that the whole course of the disease comprises a 
period of more than two or three years. The diagnosis is, as 
a rule, easy enough, and it is not difficult to differentiate the 
disease from progressive muscular atrophy if its duration and 
the condition of the reflexes are well borne in mind. Of the 
cause of the disease as well as of effectual means wherewith to 
combat it we are equally ignorant. 

LITERATURE. 

Charcot et Marie. Arch, de neurol., 1885, x, 28, 29. 

Kojewnikoff. Centralbl. f. Nervenheilk., 1885, viii, 16. 

De Wattewille. Neurol. Centralbl., 1886, v, 3. (Jaw-jerk.) 

Rybalkin. Centralbl. f. Nervenheilk., 1886, ix, 8. (Jaw-jerk.) 

Zacher. Neurol. Centralbl., 1886, v, 23. (Amyotrophic lateral sclerosis com- 
plicated by dementia paralytica.) 

Marie. Observations de sclerose later, amyotroph. etc. Arch, de neurol., 1887, 
xiii, p. 387. 

Musso. Rivista clinica, Juni 1887. 

Lennmalm. Upsala lakareforen. Forh., 1887, xxii, 7. 

Florand. Contribution a l'etude de la sclerose laterale amyotrophique. These 
de Paris, 1887. (" Maladie de Charcot.") 



TRANSVERSE MYELITIS. 443 

While the diseases of the cord which we have studied so 
far were confined to certain systems of fibres — in other words, 
were " system diseases " — the affection now to be considered 
does not present this peculiarity, but the process which affects 
the gray as well as the white matter is more or less widely ex- 
tended over the cross-section of the cord, forming a small 
number of large or numerous small foci. In other words, the 
disease is what we call " asystematic " or diffuse. It is an in- 
flammation of the cord, which according to its course is called 
an acute or chronic myelitis, and to which the name transverse 
myelitis has also been given. 

Pathological Anatomy. — Anatomical changes may in such 
cases be scarcely demonstrable even though the severest para- 
lytic symptoms may have existed during life. This is more 
especially true in cases of spinal paralysis due to pressure, 
occurring in consequence of disease of the vertebrae. Here 
we must assume that even moderate pressure is capable of 
bringing about a break in conduction without any destruction 
of nerve elements. Usually in cases where changes can be 
demonstrated we find a diminution in the size and an atrophy 
of the nerve fibres. The axis cylinders appear swollen and 
have lost their myeline sheath. The ganglionic cells, which 
are not affected until later, become shrunken and lose their 
processes. While thus the nerve tissue undergoes disintegra- 
tion the connective tissue increases, the meshes of the neuroglia 
become broader, and in it are seen the connective-tissue cells 
first described by Deiters, which, owing to their numerous 
processes, have also been called spider cells. In the meshes 
of the neuroglia reticulum, compound granular corpuscles are 
found which have taken up the fat and disintegrated nerve 
substance. These are leucocytes and in turn undergo, sooner 
or later, destruction. The vessels are dilated and changes are 
seen in their walls, consisting of thickening or hyaline degen- 
eration. In cases where this process has run its course in a 
comparatively short time, the cord is found at the autopsy to 
be soft and of a grayish-red color, whereas if the process has 
been slow the cord appears, in consequence of the connective- 
tissue increase, hardened, or, as we say, " sclerosed." 

Macroscopically, little is to be seen. At the most some 
portions may, when the cord is put into Miilier's fluid for the 
purpose of hardening it, look light yellow, while others are dark 
green. The former are the diseased parts, which can not be- 



444 DISEASES OF SUBSTANCE OF SPINAL CORD. 

come stained because the myeline sheaths, which are turned 
green by chromium, are absent. With this exception all in- 
formation about the pathological changes must be derived 
from the microscopical examination of fresh as well as of hard- 
ened sections. 

According to the location of the process we distinguish a 
dorsal myelitis, the most common ; a lumbar myelitis, the rarest; 
and a cervical myelitis, a relatively frequent form. In the first 
and second the upper extremities are entirely intact, while 
they are implicated if the process is situated in the cervical 
cord. 

Symptoms. — It is very natural that the clinical manifesta- 
tions of myelitis must, on the whole, very much resemble those 
which we have learned to recognize in the " system-diseases," 
and, as a matter of fact, almost all that will be described has 
already been said. Here, as there, we have to do with mo- 
tor, sensory, and trophic disturbances, with changes in the re- 
flexes and symptoms referable to the bladder and rectum. The 
motor disturbances may consist of symptoms of paralysis and 
irritation. The former are usually the more prominent of the 
two, and weakness of the legs, which sooner or later amounts 
to complete palsy, is one of the chief symptoms of a myelitis. 
As a rule, both legs are about equally affected — paraplegia ; 
sometimes one retains its strength longer than the other, ac- 
cording to the extent to which the pyramidal tracts are dis- 
eased. If not the legs but the arms are paralyzed, the lesion is 
situated in the cervical cord. The symptoms of irritation con- 
sist of twitchings, which occur sometimes spontaneously, some- 
times as the result of slight stimulation of the skin. In many 
instances the removal of the bedclothes and the change of tem- 
perature resulting therefrom are sufficient to cause quite pro- 
tracted clonic spasms of one or both legs. This and similar 
phenomena seem to be of reflex origin. 

The sensory changes are less regularly met with and are of 
less importance than the motor disturbances. There are in- 
deed cases where they are almost entirely absent or where they 
at least do not annoy the patient or do not become marked until 
relatively late in the course of the disease. They consist mostly 
of paresthesias, numbness, formication, also of decrease in sensi- 
bility, which may amount to a complete anaesthesia, varying in 
extent and situation. Actual pains, which are sufficient from 
their duration and intensity to cause much suffering to the 



TRANSVERSE MYELITIS. 



445 



patient, and which are so commonly seen, as we shall learn, in 
tabes, belong in this disease to the exceptions. In fact, we may 
say that they are usually absent or, at any rate, not at all 
severe. If we are able to detect sensory changes on the trunk 
itself, the level up to which these extend gives us valuable in- 
dications as to the seat of the myelitis. If it is in the lumbar 
cord, sensibility is intact above the navel ; if in the lower dor- 
sal, above the middle of the sternum. Sensory changes in the 
neck and upper extremities indicate the seat to be in the cervi- 
cal cord. The more prominent the sensory disturbances and 
the pains, the greater is the extent to which the gray matter of 
the posterior horns and the posterior columns participates in 
the inflammation or degeneration. 

Trophic disturbances appear when the trophic centres — 
that is, the ganglia of the anterior gray horns — are diseased. 
Thus, if we are able to demonstrate atrophy, with reaction of 
degeneration in the legs, this denotes a lesion of the gray an- 
terior horns in the lumbar cord, while the same condition in 
the arms indicates a disease of the anterior horns in the cervi- 
cal cord. The electrical examination should never be omitted 
in such cases, because it may happen that the legs present a 
certain degree of atrophy without the presence of any reaction 
of degeneration. This atrophy is, then, purely the result of 
disuse — the atrophy of inactivity. Other trophic disturbances 
or vaso-motor changes in the skin are not the rule. Herpes 
and urticarial eruptions, slight oedema and changes in the sweat 
secretion occur, but possess neither diagnostic nor prognostic 
value. 

One symptom remains still to be mentioned, because it is 
rarely wanting, but rather plays an important role in myelitis, 
and causes endless annoyance and discomfort to the patient — 
namely, the bed-sores which occur in the sacral region, and 
become the more extensive the less the care exercised in the 
nursing and for the cleanliness of the patient. This is one 
of the most important trophic disturbances, and one which, 
even with the most careful attention, can not in all cases be 
avoided. 

The condition of the skin as well as the tendon reflexes 
depends (i) on the state of the reflex arc in the spinal cord, (2) 
on the state of the fibres coming from the brain, which have 
probably an inhibitory function. If the reflex arc is normal, 
but the conduction of the inhibitory fibres interrupted, then 



446 DISEASES OF SUBSTANCE OF SPINAL CORD. 

the corresponding reflex is increased, while if the reflex arc 
is diseased the reflex is lost, no matter whether the conduc- 
tion of the inhibitory impulses be intact or not. This holds 
for the skin as well as tendon reflexes. Therefore, in cases of 
lumbar myelitis not only the skin but also the tendon reflexes 
are diminished or lost in the lower extremities. Those con- 
cerned are the patellar reflex, the reflex arc of which corre- 
sponds to the cord between the second and fourth lumbar 
nerves ; the tendo-Achillis reflex, the arc of which corresponds 
to the first sacral nerve ; the cremasteric and abdominal reflexes, 
which have their arc at the level of exit of the first lumbar and 
a portion of the cord between the fourth and seventh dorsal 
nerves respectively. On the other hand, in a dorsal or cervical 
myelitis a marked increase of the tendon and skin reflexes of 
the lower extremities takes place, because the (supposed) in- 
hibitory influences are cut off. 

A symptom which, perhaps, causes the patient himself more 
annoyance than any other is the disturbance in the functions of 
the bladder, which in a myelitis is hardly ever totally absent. 
At first there is some difficulty in micturition, which may end 
in complete retention, so that the patient can not void his 
urine, but requires to be catheterized. In the later stages of 
the disease, however, the urine is passed involuntarily, there 
being either a constant dribbling — incontinentia urinse — or 
from time to time an involuntary evacuation of the bladder. 
In either case the patients can not dispense with a portable 
urinal. Occasionally there is a painful burning sensation when 
the urine is passed — ischuria — so that the patient dreads every 
evacuation of the bladder. As might be expected, cystitis fre- 
quently develops in these cases, partly owing to the length of 
time that the urine remains in the bladder, partly owing to the 
frequent use of the catheter. The rectal symptoms consist 
either of a most obstinate constipation, or, if the sphincter ani 
becomes paralyzed, of incontinence of fasces (incontinentia alvi), 
which aggravates to a very serious extent any bed-sore that 
may be present. For the localization of the myelitic process 
neither bladder nor rectal svmptoms can be used. They are 
always present at whatever level the lesion may be. 

./Etiology. — Of the aetiology of myelitis little is known. It 
seems justifiable, however, to divide the causes into those 
which act chemically and those which act mechanically, the 
former being either of an infectious or of a toxic nature. That 



TRANSVERSE MYELITIS. 



447 



infectious diseases may produce myelitis is shown by the fact 
that it occurs occasionally after diphtheria, more frequently 
after small-pox, and also during the course of syphilis, and that 
the influence of poisons may at least favor the development of 
myelitis has been upheld since the action of arsenic, of mer- 
cury, and of lead, and the symptomatology of the resulting in- 
toxications have been more accurately studied. We shall later 
return to this. Among the mechanical causes the most impor- 
tant is pressure, which can be exerted upon the cord by struc- 
tures surrounding it, as happens, for instance, in spinal menin- 
gitis and meningeal tumors. Of greater importance in this 
connection is the chronic caries of the vertebrae (malum Pottii), 
spondylarthrocace, the tubercular spondylitis, and carcinoma 
of the vertebras (cf. Figs. 154 and 155), in which either the dis- 




Fig. 154- Fi g- 155- 

Complete Interruption of Conduction of the Spinal Cord during Life. Fig. 
154, anterior, Fig. 155, posterior aspect of the spinal cord. The dura mater is divided 
and folded back. Circular compression and narrowing of the spinal cord at K in conse- 
quence of carcinoma of the vertebrae in a woman thirty-four years of age. Natural size. 
The drawing is made from a fresh preparation. (After Eichhorst.) 



located (diseased) vertebrae themselves or the caseous and 
inflammatory products which are found between the dura and 
the bone may exert a compressing influence. That there are 
still other causes which may give rise to myelitis we do not 
deny ; we would only mention bodily fatigue and exposure to 
cold, but these are infinitely rarer. On the other hand there 
exists not the smallest ground for the assertion that sexual 
excesses ever produce it. 

Course. — The course in general is the following : After the 
patient has for weeks and months managed with difficulty to 



448 DISEASES OF SUBSTANCE OF SPINAL CORD. 

get around, his legs becoming weaker and weaker, he has to 
take to bed or to the rolling chair, where he spends one, two, 
even four years, harassed by various afflictions, among which 
the bladder symptoms and the motor disturbances are espe- 
cially prominent. Recovery, if it occurs at all, is only very 
exceptional, and the prognosis must, therefore, always be very 
unfavorable. Death occurs in consequence of bed-sores, which 
are seldom absent, or is at least precipitated by them. Some 
patients die from intercurrent diseases, others from the cystitis. 
The course of the so-called pressure myelitis and its resulting 
pressure paralysis, the symptoms of which have before been 
alluded to on page 314, is so far characteristic that we can 
here distinguish a prodromal stage, a stage of irritation, and a 
stage of paralysis. The prominent features of the first are 
rigidity of the vertebral column, dull, vague pains in the back, 
and the first signs of a commencing deformity. In the second 
stage we have severe neuralgic pains, hyperassthesias, par- 
assthesias, and girdle sensations. In the third, finally, paralytic 
symptoms, increased reflexes, vaso-motor and trophic disturb- 
ances (herpetic eruptions, muscular atrophies, bed-sores, etc.). 
This distinction, however, is only possible in isolated cases. 
Bladder and rectal symptoms are absent in no case of pressure 
paralysis. 

In our prognosis we must not leave out of consideration 
the possibility that the inflammatory new formations in the 
vertebras may disappear, and thus, the cause which produced 
the break in the conduction ceasing to act, it may be possible 
for the spinal cord to recover completely all its normal func- 
tions, provided, of course, that none of the nerve elements have 
been destroyed. 

Treatment. — The treatment of any case of myelitis neces- 
sitates much patience on the part of the sufferer, because weeks 
and months may pass before any sign of improvement can be 
perceived, and much circumspection on the part of the phy- 
sician, because we are never able to say beforehand how cer- 
tain measures are going to be borne by the patient, and because 
what often helps one is harmful to another; hence one must 
proceed carefully and systematically, and, as it is likely that 
the course of the disease is going to extend over years, one 
should always have something new and as yet untried in re- 
serve. If the diagnosis has once been made with certainty, it 
is our duty to inform the patient in a delicate way of the true 



TRANSVERSE MYELITIS. 



449 



state of affairs, and how seriously his capacity for following his 
occupation will be interfered with ; further, to see that he is 
properly fed on a nourishing diet and obtain for him as far as 
possible mental and bodily rest. It is a gross error to recom- 
mend such patients, who are easily fatigued and who on the 
slightest provocation are attacked by all sorts of pains, to take 
as much exercise as possible, or even to prescribe gymnastics 
for them. 

The electrical treatment is indicated and ought to be begun 
early. The constant current should be applied near the seat 
of the lesion (the anode being placed on the tender parts of the 
spinal column if there be such), the faradic to the peripheral 
parts, especially the lower legs. Definite rules can not be laid 
down. It is best to seek information from a reliable text-book 
— e. g., Erb — and to try which mode of treatment is best borne 
by the patient, and by which most is accomplished. Tepid 
baths — 84° to 88° Fahr. — three or four times a week for from 
fifteen to thirty minutes, best taken in the forenoon, usually 
have a favorable influence, and are, if not of lasting benefit to 
the patient, frequently productive of at least a transient feeling 
of comfort. The addition of rock-salt, sea-salt, or lye (one or 
two quarts) should only be ordered if the patient himself seems 
to lay much stress on it, as we can not expect any especial 
effect from them. Neither should we raise our expectations 
too high when we recommend warm brine baths containing 
carbonic acid gas, or non-medicated warm baths, or mud baths 
and the like. Of course every patient, rich or poor, expects 
us to send him in summer to the springs, but he will gradually 
find out that the success attained does not compensate for 
the expense and the trouble which the yearly course at such 
places entails, and that it is wiser to remain in his comfortable 
home or to betake himself into the country and enjoy the 
mountain or forest air somewhere where he can live in peace. 
The life in modern watering-places is not adapted for a patient 
with myelitis. Mild cold-water treatment in an intelligently 
conducted sanitarium (Graefenberg, Nassau, Elgersburg, and 
others) may well be recommended. All internal medicines 
(strychnine, silver, ergotine, iodide of potassium, etc.) are of no 
avail. The treatment of the retention of the urine and the 
consequent cystitis must be carried out according to strict sur- 
gical principles. In the treatment of a compression myelitis 
we must not forget the necessary extension apparatus, braces, 
29 



45o 



DISEASES OE SUBSTANCE OF SPINAL CORD. 



etc., for the vertebral column. These means, however, belong 
to the domain of orthopaedic surgery. 

Sometimes the effect of a unilateral section of the spinal 
cord, where we consequently again have a lesion of the gray as 
well as the white matter, can be observed in those rare in- 
stances in which traumatism, a tumor, or the like has rendered 
the half of the cord incapable of performing its functions. The 
clinical picture resulting from such a lesion is much more 

rarely observed than we 



M 




s v.vfs.m 

J_ JL it 



should be led to suppose 
from the accounts in the 
text-books. The disease 
is called Brown-Sequard's 
spinal paralysis. It, in 
short, manifests itself as a 
motor paralysis on the 
side of the lesion, and a 
sensory paralysis on the 
opposite side. This is ex- 
plained by the distribution 
of the fibres, inasmuch as 
the sensory fibres cross 
over to the other side soon 
after their entrance into the 
cord, while the motor fi- 
bres pass upward to the 
medulla oblongata without 
crossing (cf. Fig. 1 56); thus, 
if, for instance, the lesion 
be in the right half of the 
lumbar cord, a paresis of 
the right leg ensues, while the left is anaesthetic ; if the lesion is 
high up in the right half of the cervical cord, the right arm and 
right leg are paralyzed (" spinal hemiplegia "), and the other half 
of the body is anaesthetic. The fact that on the side on which 
there is motor paralysis there is often a hyperaesthesia to be 
found for certain qualities of sensation — with the exception of the 
muscular sense, which appears diminished — is explained, ac- 
cording to Brown-Sequard, by the fact that the fibres for the 
muscle sensibility do not cross over as the other sensory fibres. 
Above the hyperaesthetic there is an anaesthetic zone, due to 




Fig. 156. — Schema of the Course of the 
Nerve-fibres in the Spinal Cord, v, un- 
crossed motor fibres. v\ uncrossed vaso-motor 
fibres, sm, uncrossed fibres for the muscular 
sense, s, decussating sensory fibres. (After 
Brown-Sequard.) 



ARTERIES OF THE SPINAL CORD. 45 T 

the destruction of the posterior nerve roots. Further, there is 
an increase of the reflexes on the side affected with motor 
paralysis, owing to the cutting off of the inhibitory influence, 
as well as a vasomotor paralysis, manifesting itself by an eleva- 
tion of temperature. On the anaesthetic side the reflexes are 
normal ; a narrow hyperassthetic zone (on the trunk) is here 
also noticeable above the area of anaesthesia. 

On the whole, the descriptions which we possess of uni- 
lateral cord lesions are of no great practical use, because, as 
has been stated, the clinical picture just described is but rarely 
distinct and complete, and may present all kinds of variations 
(cf. Hoffmann, Deutsch. Arch. f. klin. Med., 1886, 38, 6, where 
three cases of this class which occurred in Erb's clinic are 
described). 

LITERATURE. 

Peabody. New York Medical Record, February 5, 1883, xxiii. 

Charpentier. Revue d'hyg., March 3, 1883, v. 

Barlow. Lancet, November 20, 1886, ii. (Myelitis after measles.) 

Grasset et Estor. Myelite cervicale. Revue de med., 1887, vii, 2. 

Schiitz. Prager med. Wochenschr., 1887, xii, 38. (Cure of myelitis.) 

Cramer. Arch. f. Psych, u. Nervenkrankh. , 1888, xix, 3, p. 667. 

Kroger. Beitrage zur Pathologie des Riickenmarkes. (Recovery from com- 
pression paralysis.) Dorpat, 1888. Inaug. Dissert. 

Gessner. Arch. f. Augenheilk., 1888, xix, 1. (Myelitis acuta after loss of 
blood.) 

II. Spinal Lesions regarded from their Pathological 
Aspect— Pathological Diagnosis. 

i. affections of the spinal cord due to diseases of the 
blood-vessels. 

A. Diseases of the Arteries of the Spinal Cord and their Consequences. 

The vertebral arteries which arise from the subclavian, and which 
unite to form the single basilar artery, give off, after having entered 
the skull, an anterior spinal and a posterior spinal artery by which 
the spinal cord is supplied with blood. The anterior spinal arteries 
of both sides unite to form a vessel which runs along the spinal cord 
in the anterior spinal fissure, while the posterior spinal arteries anas- 
tomose freely with each other without, however, completely uniting ; 
the horizontal branches run along the septa. White and gray matter 
are nourished in the same way, but the capillary network of the 
latter is much denser than that of the white substance. 



452 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



The venous blood is collected into two fairly large veins, which 
are called the central veins of the spinal cord. They anastomose 
freely among themselves, and are connected with the anterior and 
posterior spinal veins. From them the venous blood passes into the 
vertebrals, which empty into the innominate or the subclavian vein. 
About the diseases of the spinal veins up to the present nothing is 
known. 
i. Spinal Hemorrhage — Hcemorrhagia {or Apoplexid) Medulla 
Spinalis — H&matomyelia. 

While, as we have shown above, a primary haemorrhage 
from the cerebral vessels is one of the most common causes 
of lesions of the brain, spontaneous haemorrhages from the 
spinal arteries are exceedingly rare, and indeed it seems hardly 
possible that a haemorrhage could take place into the sub- 
stance of the cord, so firmly held together as it is by the tough 
pia mater, without the previous existence of alterations in its 
consistence ; besides, the anatomical conditions of the arteries 
are such that the blood pressure is decidedly lowered before 
the blood wave reaches the spinal cord ; furthermore, and this 
is, perhaps, the most important reason for the rare occurrence 
of haemorrhage into the cord, miliary aneurisms, which in 
the brain are the most frequent source of haemorrhage, are 
never found here. For these reasons the existence of primary 
spontaneous spinal haemorrhages has been absolutely denied, 
and it has been assumed that in every case changes in the con- 
sistence of the cord substance must have preceded. We fully 
agree with those who believe in their extreme rarity, but, 
nevertheless, we are of the opinion that under certain condi- 
tions primary haemorrhages actually do occur. Such condi- 
tions are : (i) in old persons the coexistence of cerebral haem- 
orrhages in consequence of arterial disease ; (2) the presence 
of such aetiological factors as excessive muscular exertion 
(heavy lifting, cutting' wood, etc.) ; (3) the sudden and violent 
suppression of haemorrhages in other places (the menses, haem- 
orrhoids, etc.) ; (4) the exposure to a sudden marked diminu- 
tion of atmospheric pressure, as happens to those who follow 
certain occupations, as, for instance, workers in compressed 
air in building bridges or winning amber (cf. Hirt, Gewerbe- 
krankheiten im Handbuch der spec. Pathologie und Therapie, 
vol. 1, 3d edition, reprint, pp. 83 et sea.). 

The pathological condition is either one of capillary haem- 
orrhages or of a haemorrhagic infiltration in which the escaped 



H^EAIA TOM YE LI A . 4 5 3 

blood extends between the nerve fibres along the course of the 
vessels, or finally we have haemorrhagic foci, in which the 
blood coming from the vessels in larger quantities presses the 
nerve tissue apart and forms a sort of cavity. The focus usu- 
ally extends in the longitudinal direction of the cord. Haem- 
orrhage may occur at any level of the spinal cord, and in any 
portion of the cross-section, and may produce the same changes 
in its substance as cerebral haemorrhage produces in the brain, 
— changes with which we have become familiar in a previous 
chapter. 

Clinically, spinal apoplexy is characterized by paralysis 
with a sudden onset, sometimes attacking the patient without 
any premonition and while he is apparently in the best of 
health ; he suddenly sinks to the ground without losing con- 
sciousness, and is deprived of the use of his limbs ; occasion- 
ally prodromata, such as tearing pains, formication in the 
limbs, may precede for hours or days. The extent and the 
degree of the paralysis depend entirely on the seat of the 
haemorrhage ; it may be confined to one half of the body or to 
both legs or to both arms, or it may take in all four extremities 
simultaneously. It develops extremely rapidly, and reaches its 
fullest extent within twenty-four hours. If this is not the case 
it is not a spinal haemorrhage with which we are dealing. Pains 
and rigidity of the back and clonic muscular twitchings are 
equally constant, as are the bladder symptoms, which are prob- 
ably never absent in haematomyelia. With regard to sensation 
and the reflexes no general rule can be given, yet an increase 
of the reflexes immediately after the catastrophe is not exactly 
rare. Death may occur within a few hours, an event which is 
especially likely to take place if the haemorrhage is situated 
high up. In other cases the patient lives for days and weeks 
and finally dies from the effects of bed-sores, of a cystitis, etc. 
Finally, at least relative recovery is not excluded ; the patient 
may either get over the effects of the lesion, or he may be left 
Avith motor or sensory disturbances of the most varied kinds. 
The differential diagnosis between haematomyelia and haema- 
torrhachis (meningeal apoplexy) has been discussed above. For 
the treatment we may try the application of ice to the spinal 
column and the internal administration of ergotine. The suc- 
cess of these measures is always very doubtful, and a careful 
attention to the nutrition and the cleanliness of the patient 
should in all cases be considered the thing of most importance. 



454 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



2. Embolism and Thrombosis of tlie Spinal Arteries and 
Myelomalacia. 

Embolism of the spinal cord, the development of which has 
been studied experimentally by Panum, is extremely rare in 
man, probably owing to the smallness of the spinal arteries and 
the fact that they arise at right angles. The symptoms by 
which emboli manifest themselves are not definitely known ; 
possibly there is a connection between embolic processes and 
the so-called choreic movements, but this is still hypothetical. 

It is about the same with arterial thrombosis, the independ- 
ent existence of which is, to say the least, doubtful, but since, 
as Leyden has pointed out (Riickenmarkskrankheiten, ii, 41), 
disease of the spinal vessels is extremely common, the occur- 
rence of arterial thrombosis is very easily possible. Not only 
the inflammatory processes in the spinal cord, which are ac- 
companied by arterial disease, but also the senile changes, 
which consist in fatty degeneration and thickening of the ves- 
sel walls, predispose to it. The necrosis which occurs in the 
substance of the spinal cord in consequence of arterial obstruc- 
tion is similar to that described on page 247 as occurring in 
the brain substance. The condition of softening is called mye- 
lomalacia. 

j. Endarteritis {syphilitica). 

That the spinal arteries participate in the process which 
Heubner has shown to occur in the cerebral arteries (page 
252), according to competent observers, does not seem to ad- 
mit of doubt. It is equally certain that this process plays here 
a relatively smaller role than in the brain. Heubner himself, 
Knapp, Leyden, and others have reported interesting observa- 
tions bearing on this, and it seems that an endarteritis obliter- 
ans in the spinal cord leads either to a myelitis or a multiple 
sclerosis. Rumpf, in his excellent treatise on The Syphilitic 
Diseases of the Nervous System (page 349), has published in 
full a very interesting case of syphilitic disease of the spinal 
arteries, which was followed by a similar report by Knapp 
(Neurol. Centralblatt, 1885, 21), and another by Graeff (Arch, 
f. Psych, und Nervenkr., 1882, xii, 3). There are, however, 
only comparatively few cases to be found in the literature, and, 
in almost all, syphilis of the brain coexisted with syphilis of 
the spinal cord, and endarteritis obliterans was almost always 



ENDARTERITIS SPINALIS. 



455 



demonstrable in the brain as well. Lately two interesting 
cases of Schmaus have appeared (Deutsch. Arch. f. klin. Med., 
1889, vol. xliv, 2, 3, p. 244). In one of them the syphilitic af- 
fection took the form of an arterial disease, running a subacute 
course with hyaline fibrous thickening of the intima and simul- 
taneous inflammatory infiltration of the whole vessel wall, 
which was followed by an irregular disseminated patchy scle- 
rosis of the white matter, a marginal sclerosis, and a degenera- 
tion of Goll's columns in the cervical cord. That the degen- 
eration of the nerve parenchyma was attributable to the low 
state of nutrition in consequence of diminution in the blood 
supply seemed beyond doubt. As for the symptoms, sensory 
disturbances (pains, paresthesias, hypersesthetic zones) and 
motor disturbances (at first fatigue and finally complete para- 
plegia), furthermore incontinence of the urine and fasces, con- 
stituted the clinical picture. In the second case a syphilitic 
degeneration of the vessel walls combined with a poliomyelitis 
was found. With our present knowledge we must content our- 
selves with diagnosticating a diffuse affection of the spinal 
cord, a transverse myelitis, a tumor, and the like. The diag- 
nosis of a syphilitic disease of the arteries must be made with 
reservation during life, and must only be assumed when the 
luetic history is certain. 

./. Dilatation of the Spinal Arteries. 

We know very little about aneurisms of the spinal arteries. 
Besides the case reported by Liouville, which is also quoted by 
Leyden (Joe. cit., 2, p. 42), none can be found in the literature. 
The question, therefore, whether syphilis may give rise to 
aneurisms here can not be answered. It is possible that bodily 
exertion has a predisposing action. A symptomatology and 
a therapy do not exist for aneurisms of the spinal cord. 

5. Neuroses of the Spinal Arteries. 

The vaso-motor nerves of the spinal arteries behave just 
like those that supply the cerebral vessels, and upon whether 
they are in a state of irritation or in one of paralysis the amount 
of blood in the spinal cord depends. But easy as it is to dem- 
onstrate hyperasmia and anasmia of the cord in the cadaver, it 
is difficult, on the other hand, to say in what way changes in 
the amount of blood in the spinal cord influence the health of 
the patient, and whether a greater or lesser fullness of the ves- 



456 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



sels, or frequent fluctuations between the two, are attended 
with any marked symptoms. All views on this subject are 
entirely hypothetical. The pathological changes in the spinal 
cord, due to an artificial transient anaemia produced by liga- 
tion of the abdominal aorta, Spronek (Arch, de physiol. norm, 
et pathol., September i, 1888, xx), following out the early re- 
searches of Brieger and Ehrlich, has lately demonstrated, with- 
out, however, throwing any further light upon the clinical 
symptoms caused by spinal anaemia. 

Since the time of Peter Franck (1791) there has been a wide- 
spread opinion that hyperemia of the spinal cord can give 
rise to a number of symptoms of irritation, some of which 
being motor, some sensory, together make up the clinical pic- 
ture of what has been described as spinal irritation. Although 
we are at present not able always to sharply identify " spinal 
irritation " as a clinical entity, and although so much ignorance 
has undoubtedly been cloaked by this term, especially of late 
years, still we can not dispense with it where we wish to de- 
scribe a certain combination of symptoms. The patients, who 
as a rule are females belonging to the best classes of society, 
complain of an occasional feeling of fatigue and of pains in 
the back, which are intensified by the erect posture. Walking 
becomes difficult, and the gait is that of an old person ; they 
walk with a bent back and take each step with care. Painful 
sensations, paresthesias, formication, and numbness in the lower 
extremities are complained of. The functions of the bladder 
are more or less disturbed ; often there exists a uterine catarrh. 
The patient is low-spirited, and has a tendency to hypochon- 
driacal notions. On examination, we find the reflexes either 
normal or exaggerated ; sensibility is somewhat affected, and 
disseminated anaesthetic plaques are demonstrable. A certain 
tenderness over the vertebrae is almost always noted ; it is 
usually more pronounced in the lumbar and dorsal than in the 
cervical region. The course of the disease is eminently chronic ; 
often months and years pass before, notwithstanding all thera- 
peutic measures, any decided improvement occurs, and those 
unfavorable cases in which the patient finally becomes bed- 
ridden and, after having been for years affected with paresis 
or paralysis, falls at last a prey to an intercurrent malady, are 
by no means exceptional. A cause is often looked for in vain. 
It is true, overexertion or sexual excesses may sometimes in- 
directly give rise to the disease ; it is true, we are at times 



spinal irritation: 



457 



justified in blaming to some extent the immoderate indulgence 
in tobacco, but more frequently all such factors are wanting, 
and we are forced to attribute it to a congenital weakness of 
the nervous system.. 

The diagnosis is not always easy, and many a myelitis prob- 
ably has been taken for spinal irritation, or more frequently, 
perhaps, spinal irritation has been mistaken for myelitis. Only 
in the cases, which are not rare, in which remissions lasting for 
months occur, so that the patients begin to have hopes of a 
speedy and complete recovery, the diagnosis is not doubtful. 
Sometimes it may not be possible to make it at all. 

The treatment should be local and general. The former 
consists in the early and energetic use of the Paquelin cautery 
and of the constant current (descending) ; the latter in the 
use of tepid baths and tonics. Yet often all measures are 
fruitless, and it is advisable to be very guarded in giving an 
opinion with regard to the duration and probable outcome of 
the disease. 

That a chronic anaemia of the substance of the spinal cord 
may give rise to a paralysis, especially of the lower extremi- 
ties, which may last for years, seems probable according to the 
thesis of Meunier (Paris, 1886), yet nothing certain can be said, 
especially as in the cases in question it may be difficult to ex- 
clude hysteria. 

Just to what class we must assign those instances of paral- 
ysis, described more especially by Russell Reynolds, which 
depend on the imagination — whether they are due to func- 
tional disturbances in the spinal cord, or whether, under the 
influence of psychical activity in consequence of auto-sugges- 
tion, a disease of the whole nervous system develops — is not 
known. 

The various disturbances in the sexual functions — for in- 
stance, the impotentia coeundi, which is quite a common mani- 
festation of a functional disturbance of the spinal cord in young 
and middle-aged men — we shall enlarge upon in the chapter 
on neurasthenia. 



458 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



II. INFLAMMATORY PROCESSES IN THE SUBSTANCE OF THE 
SPINAL CORD. 

/. Purulent Myelitis — Abscess of the Spinal Cord. 

While circumscribed pus formations in the brain substance 
are by no means rare, the formation of an encapsulated pus 
focus in the spinal cord is one of the greatest exceptions. Al- 
though Leyden succeeded in producing such foci experiment- 
ally in dogs, the clinical observations in man are so few that it 
is impossible to formulate from them a definite symptoma- 
tology. Pathologically, it is interesting to note that Ollivier 
and Jaccoud (quoted by Leyden, loc. cit., ii, 205) have seen ab- 
scesses which varied in size from that of a bean to that of a 
hazel-nut and were filled with a greenish-white pus. They were 
situated some in the cervical, some in the dorsal cord. The 
symptoms, on the whole, were those of a grave, acute soften- 
ing. In a recent article of Ullmann (Zeitschr. f. klin. Med., 
1889, xvi, 2, page 39) an interesting discussion on spinal ab- 
scesses and an exhaustive collection of references will be 
found. 

2. The Non-purulent Myelitis. 

Inflammatory processes in the spinal cord are very fre- 
quent. In the majority of cases they are of a chronic type 
and less often acute. With reference to their situation we 
have already stated that they may implicate the white as well 
as the gray matter. 

A. The Acute Form. 

As we said on page 443, we have in acute myelitis a process 
which is characterized by the death of the nerve elements and 
a secondary increase of the connective tissue. In the acute 
stage a change in the consistence of the cord takes place ; the 
parts become softened and appear swollen and infiltrated. Sec- 
tions of the cord are not so distinct, and the demarcation be- 
tween the white and gray matter is less sharp. The color may 
be reddish (hemorrhagic), yellowish-red, rusty brown, whitish, 
or of any intermediate shade. The extent of the process of 
softening varies. It may be spread over the whole or only a 
part of the cross-section, and may extend longitudinally for a 
greater or less distance. Sometimes disseminated foci are 



LANDRY'S PARALYSIS. 



459 



found not only in the cord, but can also be demonstrated in 
the brain. We shall speak about these later. 

In exceptional cases, which are difficult to explain, abso- 
lutely no changes were found at the autopsy, although the 
course of the disease seemed in every way to suggest an acute 
lesion. These patients were, for the most part, young and up 
to the time of their illness vigorous persons. After a short 
prodromal stage, in which there was headache and some fever, 
they were attacked by a flaccid paralysis of both legs, which 
developed in a few days. To this was added in a very short 
while paresis of both arms, so that the helplessness of the pa- 
tients reached an unusual degree. The condition of the reflexes 
and the electrical excitability varied in the few cases reported 
up till now. According to the records, the functions of the 
bladder and rectum as well as sensibility remained normal. 
The prognosis is very doubtful. Sometimes bulbar symptoms 
appear and the patient dies within from eight to fourteen days 
after the onset. Sometimes the course is more protracted and 
some improvement occurs, which, however, is never complete. 
The affection, which presents the clinical picture just described, 
is called Landry's paralysis (1859), paralysie ascendante aign'e, 
acute ascending spinal paralysis, although it is not definitely 
known whether we actually have to deal with a spinal af- 
fection and not rather with a very acute infectious peripheral 
neuritis. Until we possess the results of a larger number of 
anatomical examinations it is no use to theorize any more about 
the nature of the disease (cf. Schultze, Schwarz, Bernhardt, 
etc.). 

With regard to the aetiology of acute myelitis, all that is 
necessary has been stated on page 447. The influence of cer- 
tain poisons in causing changes in the spinal cord, more espe- 
cially the so-called intoxication paralyses, will be discussed in 
the chapter on the diseases of the general nervous system. It 
is possible that Landry's paralysis, about which so little is 
known, can be caused by infectious diseases, for instance by 
whooping-cough (Mobius). Of great interest is the communica- 
tion of Curschmann (Verhandl. des fiinften Congresses fur innere 
Med., Wiesbaden, 1886, page 469), in which he speaks of a case 
of acute ascending paralysis where at the autopsy typhoid 
bacilli were found in the spinal cord. Further, it has been 
known to follow working in great heat (Prahl, Hosp. Tidende, 
1876, 2 R., iii). Often no ^etiological factor can be made out. 



460 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



The symptomatology, diagnosis, and treatment of acute 
myelitis have been discussed on pages 444 to 449. 

LITERATURE. 

Schultze. Berl. klin. Wochenschr., 1883, 39. 

Hoffmann. Areh. f. Psych, und Nervenkr., 1884, xv, I, 140. 

Bernhardt. Zeitschr. f. klin. Med., 1886, p. 391. 

Pitres et Vaillard. Arch, de physiol. norm, et pathol., fevr. 1887, p. 149. . 

Lewtas. Lancet, August 13, 1887. 

Dixon Mann. Brit. Med. Journ., March 26, 1887. 

Iwanow. Zwei Falle von acuter aufsteigender Spinalparal. Petersb. med. 

Wochenschr., 1888,46. 
Schwarz. Zeitschr. f. klin. Med., 1888, xiv, 3, p. 293. 
Lorentzen. Ugeskr. f. Lagev., 1888, 4 R., xvii, 33. 
Moller. Ibid., 1888, xviii, 4, 5. 
Woodward. Brit. Med. Journ., November 3, 1888. 

B. The Chronic Form. 
Chronic myelitis is much more commonly observed than 
the acute form. It is characterized by the death of the nerve 
elements and a consequent increase of the connective tissue, 
which gives to the tissue a peculiar firm appearance and con- 
sistence — sclerosis. That this sclerosis is frequently confined 
to certain nerve tracts, giving rise to the so-called " system-dis- 
eases," we have pointed out above on page 435. On page 444 
will be found some account of the sensory, motor, and trophic 
changes which are found in these affections. It is in all cases 
of great importance to look to the condition of the reflexes, as 
this may have a decisive significance for the diagnosis. The 
disturbances of the bladder and rectum in chronic myelitis and 
the treatment of the disease have been discussed above. 

III. Spinal Tumors. 

Pathological Anatomy, — In the spinal cord, just as in the 
brain, the glioma is relatively the most frequent form of pri- 
mary neoplasm. What has been said on page 288 about its 
development holds good here also. The cervical and dorsal 
part of the cord seem by preference to be the seat of the gli- 
oma. Sarcomata, which from the onset present a sarcomatous 
nature, and gliosarcomata — that is, gliomata with unusually 
marked proliferation of cells — have been observed, although 
but rarely as primary tumors. Angiomata, small reddish, 
probably congenital (Virchow) foci, have been found, and Gan- 



SPINAL TUMORS. 4 6i 

guillet has observed a cylindroma in the lowest portion of the 
spinal cord. Solitary tubercles and syphilomata are much 
rarer here than in the brain. Carcinomata usually start from 
the vertebrae and afterward spread to the spinal meninges. 
The secondary changes are, of course, not nearly so well 
marked here as those we find in the brain, since the spinal cord 
is in a position to offer greater resistance to the growth that 
presses upon it. Only when the tumor has reached some con- 
siderable size — e. g., that of a hazel-nut— do symptoms analo- 
gous to the so-called "indirect symptoms" in the brain make 
their appearance. 

etiology. — The aetiology is absolutely unknown. Though 
in certain cases traumatism has been made responsible for 
gliomata in the spinal cord, we are still in complete igno- 
rance about the real cause, as we confessed ourselves to 
be when treating of their occurrence in the brain. The in- 
fluence of age and sex here is the same as in tumors of the 
brain. 

Symptoms. — If a patient complains of persistent pains and 
stiffness in his back, if at the same time there are found sensory 
disturbances in the form of paresthesias, circumscribed areas 
of anaesthesia, and motor disturbances in the form of slowly 
but steadily progressing paralysis of one or more extremities, 
the suspicion, that a tumor of the meninges or of the cord itself 
exists, is justifiable. The likelihood is greater if other spinal 
affections can be excluded and if occasional remissions in the 
progress of the disease can be noted. It is true the diagnosis 
of spinal tumors always remains a very difficult thing, and at 
times, for instance, we may not be able to definitely differenti- 
ate a myelitis from a spinal tumor. This is easily understood 
if we consider that spinal tumors may give rise to the most 
varied clinical pictures, according to their position and size 
and according to the greater or lesser involvement of the 
white or gray matter. There is no doubt but that a tumor 
of the spinal cord may give rise to symptoms of a compres- 
sion myelitis, of tabes, or of a myelitis, and that if it be con- 
fined to one side it may produce the symptoms of a Brown- 
Sequard's paralysis. Roth (cf. lit.) claims that loss of the tem- 
perature sense is frequently observed in spinal glioma, and 
that this, combined with analgesia, paresis, and muscular 
atrophy, is sufficient to settle the diagnosis. The considerable 
material which Roth has at his disposal makes his monograph 



462 DISEASES OF SUBSTANCE OF SPINAL CORD. 

very valuable. It is only to be expected that vaso-motor 
as well as trophic symptoms should be found. To interpret 
these must be left to the physician's skill in diagnosis, upon 
which so much depends in the recognition of tumors of the 
cord. Sudden changes in the spinal symptoms, temporary re- 
missions, then again sudden changes for the worse, should all 
be made to have their proper diagnostic value. In cases of 
well-marked paraplegia dolorosa, where we have tearing pains 
in the small of the back, radiating into the extremities, to- 
gether with atrophy of the muscles of the lower legs, we 
should always think of one or several tumors of the cauda 
equina. In these cases contractures of such severity sometimes 
develop that the heels touch the buttocks (Leyden). 

Prognosis. — The prognosis depends upon the nature and 
the seat of the tumor, although the ultimate outcome is always 
unfavorable. If the growth be benign and be situated in a 
relatively indifferent area, the patient may last for years, and 
even enjoy periods so free from discomfort that he may deem 
a recovery quite possible. 

Treatment. — The treatment can only then be of any avail 
if surgical interference — that is, excision of the tumor — is pos- 
sible. A case of this character has been reported by Gowers 
and Horsley. An oval myxoma which had pressed upon the 
cord was, after removal of the spinous processes of the third, 
fourth, and fifth dorsal vertebra?, excised, and the patient re- 
covered completely. Bruce and Mott (cf. lit.) diagnosticated 
intra vitam a tumor which, originating in the fifth left dorsal 
nerve, pressed upon the middle of the dorsal part of the spinal 
cord ; the patient presented the symptoms of a compression 
myelitis and died. At the autopsy softening with ascending 
and descending degeneration was found. The authors regret 
in their paper not having decided upon an extirpation of the 
tumor. 

All other means are fruitless. If there is any suspicion that 
the case is one of syphilis, inunctions with mercury ought to 
be given a trial. 

Appendix. — Parasites in the Spinal Cord. 

About parasites in the spinal cord we may look in vain for 
information in the text-books, probably because their occur- 
rence is very unusual, and also because, if they are present, 
they may not give rise to any symptoms. But here we ought 



H YDRORRHA CHIS. 



463 



to make at least a short mention of the cysticerci which have 
been found not only in the brain, but also in the spinal cord. 
Leyden only devotes a few words to this subject in his Klinik 
der Rlickenmarkskrankheiten (1,445): "Still more rare (than 
the cysticerci in the brain), and as yet of no clinical significance 
whatever, are the cysticerci which may develop ... in the 
annexes of the spinal cord, etc." I have shown in a case which 
came to my notice, and which I have reported (cf. lit), that 
cysticerci of the spinal cord — there were fifteen or twenty in 
the dural sac — may give rise to symptoms simulating those 
of tabes ; some clinical significance has, therefore, to be attrib- 
uted to them. That the symptoms of spinal irritation, which 
are associated with such parasites in the cord, are not to be 
attributed to the increased intraspinal pressure, but that they 
are of a reflex nature, seems beyond doubt. To diagnosticate 
intra vitam the existence of intraspinal parasites is only possi- 
ble in exceptional cases — as, for instance, if the patient is a 
butcher by trade, or if his frequent indulgence in raw meat 
gives rise to the suspicion of cysticerci ; but even in the most 
favorable cases the diagnosis can not claim to be more than 
conjectural. 

Almost as rarely do we find echinococci in the vertebral 
canal. A case of this nature, however, which is of a great 
deal of interest, has been published by Jaenicke (cf. lit.). An 
echinococcus, which had existed in the subpleural tissue in the 
region between the ninth and the twelfth dorsal vertebra, pene- 
trated into the vertebral canal, and, owing to the compression 
thus exerted upon the spinal cord, gave rise to such charac- 
teristic symptoms that the diagnosis intra vitam was to a cer- 
tain degree justifiable. 

IV. Congenital Diseases — Hydrorrhachis— Spina Bifida. 

To a collection of fluid in the skull we have given the name 
hydrocephalus (page 305) ; similarly a like collection in the 
vertebral canal we call hydrorrhachis, and specify two forms of 
the disease — the hydrorrhachis externa and interna — accord- 
ing as the fluid is situated in the meshes of the pia, or between 
the meninges, or, on the other hand, in the interior of the 
spinal cord. In the latter case we find a dilatation of the cen- 
tral canal, which is either uniform throughout or beaded. 

At the autopsy we not rarely, instead of the normal central 
canal, the ordinary diameter of which measures from one 



464 DISEASES OF SUBSTANCE OF SPINAL CORD. 

tenth to one millimetre, find a canal with a diameter of two, 
five, or even ten millimetres (" hydromyelia "), or alongside of 
the usual canal abnormal cavity formations ("syringomyelia"); 
during life, on the other hand, such conditions are by no means 
often correctly recognized. The practical significance of these 
abnormities is not great, as for one thing the signs during life 
are so uncertain and changeable that a correct diagnosis has 
almost to be regarded as accidental, and, secondly, because the 
disease, even if recognized, is not at all accessible to any treat- 
ment. Notwithstanding this, it is of course desirable that the 
present state of our knowledge of hydromyelia and syringo- 
myelia should be given briefly here, and that attention should 
be drawn to the symptoms most commonly observed in these 
affections. 

With reference to the origin of hydromyelia it is especially 
abnormities in development which we have to deal with, and 
more rarely does the influence of pressure — e. g., a tumor in 
the posterior fossa of the skull — come in. For the develop- 
ment of syringomyelia central gliosis, with secondary disinte- 
gration and cavity formation, is said to play an important part. 
These cavities may connect with the fourth ventricle, and ex- 
tend through the medulla oblongata as far as the conus termi- 
nalis, and on a cross-section two or more lumina may be seen. 
They are of variable lengths, and are, as a rule, situated in the 
lower cervical and in the dorsal cord, and especially in close 
proximity to the central canal, sometimes also in the posterior 
horns. Their width varies from a half to ten millimetres; their 
contents are sometimes watery and thin, sometimes milky and 
viscid. The relation of the central canal to these cavities varies 
so much that no rule can be given on this point. In certain 
instances it remains intact in its whole length. 

Among the clinical signs there are, more especially, three 
which should arouse a suspicion of syringomyelia — namely, (1) 
localized muscular atrophies, more especially in the upper 
extremities, be it in one or in both ; (2) a widespread, non- 
typical hemianassthesia (more especially analgesia) ; and (3) 
trophic disturbances of the skin and the deeper parts (whitlow, 
phlegmon), and also of the bones, which easily break (Schultze, 
cf. lit.). The muscular atrophy is always associated with a 
more or less pronounced paralysis, as we might expect in 
lesions of the gray anterior horns. In such instances amyo- 
trophic lateral sclerosis or peripheral neuritis may suggest 



SPINA BIFIDA. 465 

itself as a diagnosis. The sensory changes we shall understand 
if we remember that the posterior commissure, Goll's columns, 
and the posterior horns are preferably the seat of the affection. 
In a case of Schiippel (Arch. d. Heilk., 1874, xv, p. 44) gen- 
eral anaesthesia was found. On the other hand, we ought not 
to omit to state that in many instances all sensory changes are 
absent, so that even this symptom is far from being pathogno- 
monic. The condition of the reflexes varies much, as does also 
the appearance of trophic and vaso-motor disturbances under 
the form of exanthematous eruptions, vesicles, ulcerations, 
erysipelatous swellings, etc., which are sometimes present, 
sometimes absent. All the cases observed up to 1887, and two 
new ones that had come under her own observation, have been 
collected and analyzed by A. Baumler (cf. lit.). 

Somewhat related to these dilatations of the central canal 
are those congenital cystic tumors which, penetrating through 
the walls of the vertebral column, make their appearance below 
the skin on the back. If the cyst, the size of which may vary 
from that of a walnut to that of a man's fist, is situated in the 
middle line over the sacrum, it is called a sacro-lumbar myelo- 
meningocele, or spina bifida. The skin over the tumor is 
normal ; below it are found the bulging dura and arachnoid. 
The contents of the sac, which has sometimes smooth, some- 
times rough walls, are as clear as water and identical with the 
cerebro-spinal fluid. The spinal cord is attached to the inner 
wall of the sac by a broad base, or at its point of entrance di- 
vides into several strands which pass directly into the wall of 
the cyst. The coexistence of a hydromyelus with a spina 
bifida, the former causing an atrophy of the substance of the 
spinal cord and a communication between the central canal 
and the cavity of the spina bifida, is a rarity. 

In a child born with spina bifida we find, as we stated, in 
the middle of the back, in the region of the sacrum, a soft, 
doughy, elastic, not rarely fluctuating, tumor, which can be 
made smaller by pressure. The position of the child influ- 
ences the condition of the sac. It is tense in the erect pos- 
ture ; when the child lies down it becomes flaccid and soft, 
a fact which must be referred to the communication usually 
existing between it and the cranial cavity. 

Although the child thus affected may at first develop fairly 
normally, his life is endangered from the first moment. Not 



4 66 



DISEASES OF SUBSTANCE OF SPINAL CORD. 



only does the pressure exerted upon the spinal cord by the in- 
creasing tumor lead to motor and sensory changes, as well as 
bladder symptoms, but there exists a constant menace to life 
which the rupture of the sac would entail, an accident which 
is favored by the gradual thinning of the overstretched skin. 
Such a rupture is almost always followed immediately by con- 
vulsions and death. 

The aetiology is not known. Possibly we have to do with 
a developmental anomaly, possibly, as Virchow believes, with 
an early formation of partial hygromata (hydromeningo- 
cele). 

The treatment of spina bifida belongs to the domain of the 
surgeon. We may either endeavor to get rid of it by repeated 
puncture and subsequent injections of a solution of iodine in 
glycerine (Morton), or we may content ourselves with methodi- 
cal compression. The whole treatment, however, should, 
owing to the danger of a meningitis, always be undertaken 
with the greatest caution. 

LITERATURE. 
i. Syringomyelia. 

Wallis. Cas d'atrophie musculaire progressive due a une hydromyelie. Arch. 

de neurol., 1885, xiv, 42, p. 405. 
Oppenheim. Charite-Annal., 1885, xi. 
Schultze. Virchow's Archiv, 1885, 102, 3, p. 440. 
Baumler, A. Deutsches Arch. f. klin. Med., 1887, xl, 5, 6. (Very complete list 

of references.) 
Joffroy et Achard. De la "myelite cavitaire." Arch, de phys., 1887, xix, 7. 
Chiari. Ueber die Pathogenese der sogenannten Syringomyelie. Zeitschr. f. 

Heilk., 1888, 4, 5. 
Roth. De la gliomatose medullaire. Arch, de neurol., 1888, 46, 47, 48. 
Schultze. Zeitschr. f. klin. Med., 1888, xiii, 6. 
Remak. E. Oedem der Oberextremitaten auf spinaler Basis. Berl. klin. Woch- 

enschr., 1889, 3. (Syringomyelia.) 
Bernhardt. Syringomyelie und Scoliose. Centralbl. f. Nervenheilk., 1889, xii, 2. 
Lemoine. De la syringomyelie. Gaz. med. de Paris, 1889, 12-14. 
Rumpf. Ueber einen Fall von Syringomyelie nebst Beitragen zur Untersuchung 

der Sensibilitat. Neurol. Centralbl., 1889, 7. 

2. Tumors, Parasites, and Spina Bifida. 

Jaenicke. Ein Fall von Echinococcus des Wirbelcanales. Bresl. arztl. Zeitschr., 

November 7, 1879, 21. 
Dollinger. Die osteoplastische Operation der Hydrorrhachis. Wiener med. 

Wochenschr., 1886, xxxvi, 46. 
v. Recklinghausen. Virchow's Archiv, 1886, Bd. cv, 2, 3. 



SPINA BIFIDA. 



467 



Brunner. Ibid., 1887, Bd. cvii, 3. 

Bruce and Mott. Case of Myxo-fibroma of the Fifth Dorsal Nerve extending 
on the Spinal Cord. Brain, July, 1887, xxxviii, p. 210. 

Hirt. Ein Fall von Cysticerken im Riickenmarke. Berl. klin. Wochenschr., 
1887, 3. 

Recklinghausen. Untersuch. iiber Spina bifida. Virchow's Archiv, 1887, 105, 
pp. 243, 275. 

Holt. Remarks upon Spina Bifida. New York Medical Journal, November 5, 
1887. 

Bland Sutton. On Spina Bifida Occulta and its Relation to Ulcus Perforans and 
Pes Varus. Lancet, July 1, 1887, li. 

Beneke. Fall von unsymmetrischer Diastemato-myelie mit Spina bifida. Leip- 
zig, 1888, Festschrift. 

Wichmann. Weiner med. Wochenschr., 1888, 24, p. 837. 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



In diseases of the general nervous system, the brain and 
spinal cord and the nerves which come off from them all share 
in the morbid process, yet the extent to which the different 
parts are implicated varies very much in different cases. Some- 
times, in so far as clinical symptoms would lead us to con- 
clude, the trouble lies mostly in the brain, sometimes in the 
spinal cord. In the latter case, again, we may have a more 
marked implication of the substance of the cord itself, lesions 
of certain tracts, or perhaps the lesions of the peripheral spinal 
nerves may come more into the foreground. Between such 
extremes there exist manifold intermediate forms, but to say 
much about the course of these diseases which would be appli- 
cable to all becomes all the less possible because a second 
point has to be taken into consideration, namely, whether, and 
if so how far, the whole organism shares in the disease of the 
nervous system. This participation varies in many ways, and 
there are diseases of the general nervous system which can ex- 
ist for years without any serious implication of the general or- 
ganism ; while there are others, and these are far more numer- 
ous, in which sooner or later the nervous disease grows, as it 
were, into a general disease, in which the organs which have to 
do with digestion, circulation, secretion, excretion, sometimes 
even respiration, are affected more or less seriously. That the 
course of the disease and the prognosis must sometimes be 
materially influenced by this we need not say, and one rule is 
forcibly impressed upon us by such cases, a rule which must 
never be lost sight of by the physician, viz., never in a case of 
disease of the general nervous system to content ourselves 
with an examination of the nervous system, but to remember 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



469 



that the same care must be devoted to all organs without 
exception. This rule, self-evident enough to the conscientious 
observer, we have dared to emphasize again because it is more 
especially in nervous diseases that it has been allowed to fall 
into abeyance. As to the pathology of the diseases which we 
are about to consider, our knowledge is unfortunately in many 
respects very scanty, and in many of them no lesions at all 
have been found after death, although the assumption, that in 
the majority of cases some anatomical changes, macroscopical 
or microscopical, must have been present, would appear to be 
justifiable. Only for certain of the diseases in this category, 
as tabes, dementia paralytica, multiple sclerosis, and certain 
chronic intoxications, have anatomical changes been demon- 
strated, and even here we are not always clear about their 
significance. Again and again it has happened that after an 
accurate analysis of the clinical symptoms a diagnosis has been 
made intra vitam and this and that anatomical change has been 
reckoned upon with certainty, and then at the autopsy the 
whole nervous system was found to be absolutely intact. 
Among such cases we may mention that of Westphal, where 
a multiple sclerosis was diagnosticated ; that of Killian, a sup- 
posed chronic myelitis ; and a certain case of ophthalmoplegia 
externa progressiva of Eisenlohr. Instead of the pathological 
condition expected, the brain, spinal cord, and their nerves 
were found to be absolutely normal. On the other hand, it 
has happened that where hysteria, epilepsy or chorea had been 
diagnosticated and one had prophesied most confidently that 
the condition of the central nervous system would be found 
normal, the autopsy has shown extensive changes — multiple 
foci in the spinal cord or in the brain cortex, recent or old 
areas of softening, etc. To such errors even the most reliable 
observer is exposed, and it is just the man who has observed 
accurately the greatest number of cases and assisted at the 
post-mortem examination of them who will be most cautious 
in his diagnosis and in his prophecies as to what will probably 
be found at the autopsy. 

Uncertain then as is the condition of our pathological 
knowledge in these cases, still, if we decide to treat of diseases 
of the general nervous system not simply one after the other, 
but to adopt some arrangement into groups, it is best to base 
this in a general way on the conditions which we find after 
death, and to distinguish two classes, the first consisting of 



47Q 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



nervous diseases in which up to the present time no anatomical 
changes have been demonstrated at the autopsy, diseases which 
we therefore call functional neuroses ; the second, those dis- 
eases which are always associated with known anatomical 
changes. 



PART I. 

DISEASES OE THE GENERAL NERVOUS SYSTEM 

WITHOUT ANY RECOGNIZABLE ANATOMICAL 

BASIS. 

" Functional Neuroses." 

The affections coming under this head are much more 
numerous than those for which an anatomical basis is known. 
Their number justifies the desire to divide these, again, into 
groups, an undertaking, however, which presents the greatest 
difficulties, because any classification must always appear to a 
certain extent forced. Inasmuch as no pathological anatomy 
enters into the question, we have here to help us only the aeti- 
ology and the symptomatology. From the former we can ex- 
pect nothing, since, as we shall see, the cause is sometimes ut- 
terly unknown, at other times so uncertain and variable that it 
does not warrant us in assigning a particular disease to any 
particular group. 

As for the second, the symptoms also present so many varia- 
tions that it is difficult to classify them ; and even if we take 
into consideration the fact that in some diseases the symptoms 
belonging to the cerebrum, in others those belonging to the 
spinal cord predominate, a distinction can not always be arrived 
at, since some symptoms, such as certain motor and sensory 
disturbances, may be of cerebral just as well as of spinal origin, 
and in a given case it may be absolutely impossible to deter- 
mine with which kind we are dealing. It only remains, then, 
if we are not willing to renounce all attempts at classification, 
to come back to the question as to what influence the neurosis 
exercises upon the general condition of the patient and to de- 
termine whether, and if so, to what extent, the general organ- 
ism shares in the nervous disease. Thus we shall find that 
some of them (though these are the few) disappear after run- 
ning a shorter or longer course without leaving behind them 



472 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



any bad effects, or again last for years, during which time the 
patient feels fairly well, or, at all events, shows no serious gen- 
eral symptoms ; while there are others that are characterized 
not only by their long duration, their obstinate resistance to 
treatment, and their tendency to recur, but also by the baneful 
influence which they exert on the general system. The former, 
for the sake of brevity, we shall designate as mild, the latter as 
grave neuroses, although we do not mean to exclude the pos- 
sibility that now and again among the ones we call mild we 
may not encounter a serious disease running a tedious course, 
while among the grave forms we may have cases by no means 
as severe as usual. We would also especially state that we are 
in no wise satisfied with our classification, and look upon it 
only as a temporary makeshift, to be superseded as soon as 
some better method has been discovered. 



FIRST GROUP. 

NEUROSES WHICH ARE WONT TO RUN THEIR COURSE WITH- 

OUT ANY ESSENTIAL IMPLICATION OP THE 

GENERAL ORGANISM. 



CHAPTER I. 

CHOREA — CHOREA ST. VITI — ST. VITUS' DANCE — BALLISMUS — MELAN- 
CHOLIA SALTANS — SYDENHAM'S DISEASE. 

By the term chorea in general we mean the occurrence of 
peculiar irregular movements entirely beyond the control of 
the patient. They appear in the upper extremities and in the 
face, as well as, though to a lesser extent, in the lower extrem- 
ities and in the trunk. They only attack the voluntary mus- 
cles and may persist for days, weeks, and even months unin- 
terruptedly, except during sleep. If these movements, as is 
frequently the case, are confined to one side only, to one half 
of the face, to one arm and the corresponding leg, we speak 
of a hemichorea. The distinction which is made in some of 
the older books between chorea major and chorea minor has 
become superfluous, since the symptoms which were formerly 
described as constituting the clinical picture of chorea major 
do not represent an independent disease, but belong to the 
domain of hysteria. Hence we can also dispense with the 
designation " chorea minor." 

The " choreic " movements may appear independently 
where it is impossible to find any coexisting symptoms of 
another disease, or they may be no more than symptoms of 
another affection, be it of the brain or spinal cord. Our exam- 
ination will have to decide between these two possibilities. 
We shall first call attention to the idiopathic, genuine chorea, 
and we need hardly say that only this form is to be regarded 
as a mild neurosis in the sense pointed out above. 

Symptoms. — To describe the choreic movements in detail 



474 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

is not easy, because they present very many varieties in de- 
gree and extent. Jn the relatively severe cases all the muscles 
participate, the head is thrown about and shaken, the neck is 
twisted, the forehead is wrinkled and smoothed, the eyelids 
closed and opened, and the eyeballs rolled around. The facial 
muscles, including those of the lips and the mouth, take part in 
the movements, thus giving rise to the most varied expressions 
— e. g., those of terror, anxiety, or joy — according to the par- 
ticular muscles most strongly affected. Hasse states that the 
tip of the nose may be moved, though I myself have never 
seen this. Very conspicuous are the movements of the tongue 
muscles, since they interfere with speaking, chewing, swallow- 
ing, and with the protrusion of the tongue, which in the worst 
cases become entirely impossible. The implication of the mus- 
cles of the trunk gives rise to rotatory and other involuntary 
movements of the body ; the patient rises and falls down again, 
and may work himself into the most peculiar and marvelous 
positions ("fotie des muscles "). 

In the great majority of cases the movements do not take 
place in the way we have described, except, perhaps, the 
twitchings of the face, but are confined to the upper extremi- 
ties, or are at any rate most marked here. Shoulders, arms, 
hands, and fingers are constantly in motion, the affected mus- 
cles twitch, the arms are extended and flexed, the fingers 
spread apart, and so forth. A similar restlessness is observed 
in the muscles of the thigh and calf, the feet are alternately 
lifted, the toes moved, etc., although the lower extremities 
are generally attacked to a lesser extent. Sometimes the 
movements are gone through with lightning quickness, in 
which rare instances the name chorea electrica is justifiable. 
In milder cases the patients may at times be able to remain 
perfectly quiet, and only slight twitchings in the arms, the 
fingers, perhaps also in the facial muscles, will betray the exist- 
ence of the disease. It is a characteristic feature of idiopathic 
chorea that all movements entirely cease when the patient is 
asleep, although going to sleep may be rendered somewhat 
difficult. Once asleep, however, such patients rest quietly, and 
are not disturbed by any muscular unrest. 

That the intended movements are influenced by the patho- 
logical ones goes without saying, and it is quite possible that 
at a time when the disease is still at its beginning and has not 
yet been recognized, but is already exerting its influence upon 



SYMPTOMS OF CHOREA. 



475 



the voluntary movements, the patient may be simply regarded 
as awkward and clumsy. If this happens to children who have 
to write in school, or recruits who have to drill and learn the 
different manipulations, much unpleasantness for the patient 
may arise from this condition, which might have been avoided 
by a careful examination by a physician. Generally the vol- 
untary movement is normal in its first phase, but soon the 
muscles begin to be seized by the spasms and the patient is 
not able to carry out the movement intended. This is noticed 
in dressing or eating, or in other ordinary actions of daily 
life, but most of all is it seen in writing, playing the piano, or 
in the performance of other movements requiring a high de- 
gree of co-ordination, and can even be marked if we ask the 
patient to put out his tongue. 

His apparent awkwardness excites the patient very much, 
and the more he tries to execute the intended movement, the 
more he tries to govern his unmanageable muscles in the usual 
manner, the less he succeeds and the more he is annoyed by 
the involuntary movements. Only a few particularly well 
disciplined patients are, at the height of the disease, able to 
keep their muscles for a few moments at absolute rest. The 
reflex and automatic movements are not interfered with. 
Protective movements are performed as by healthy persons ; 
coughing and sneezing are done normally ; neither do the car- 
diac or respiratory movements suffer. 

The sensibility is in no way interfered with. Tenderness 
over the spine may be present, although not regularly. Other- 
wise nothing abnormal can be noticed in the domain of the 
sensory nerves. It is remarkable to note that there is no sense 
of fatigue, which we certainly should expect after such excess- 
ive muscular action. The body temperature and the urine 
remain normal throughout the disease if no complications are 
superadded. On the other hand, the psychical condition of 
the patients, especially if they be young people, undergoes 
more or less marked changes, which constitute a prominent 
feature of the disease if the course be prolonged ; children who 
have up to this time been kind, obedient, diligent, and willing, 
become willful, peevish, and spiteful ; although learning nicely 
and without difficulty and making good progress in school be- 
fore they had any symptoms of chorea, they become slow at 
grasping and understanding what they are taught ; the easiest 
things must be repeated and impressed upon them, and often 



476 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



enough they are forgotten again in a few hours. If, and this 
is not rarely the case, an impediment in speech is added in 
consequence of the choreic movements of the tongue, the chil- 
dren become wholly unfit for school. It is at this time no 
longer necessary to advise keeping the child at home, since 
the teachers themselves will no longer permit it to attend. 
The influence of the disease upon the psychical functions is 
generally much less marked in adults. 

In the idiopathic uncomplicated chorea the described mani- 
festations persist usually for several weeks with varying inten- 
sity. From the onset to the cessation of the disease from sixty 
to ninety days may elapse (sixty-nine days, See ; eighty days, 
Jiirgensen; eighty -nine days, Riecke), yet, as we shall show 
later, the treatment is not without influence upon its duration. 
By far the most frequent issue is recovery, although the possi- 
bility of a relapse is by no means excluded, and in giving a 
prognosis this feature should be taken into account. Death 
from chorea is a very uncommon event, and only may occur 
in very weakly children or when complications arise ; other- 
wise we may in most cases give with a clear conscience a 
good prognosis. 

Complications. — But it is just these complications and the 
relation that chorea bears to other diseases which deserve so 
much attention, more particularly as this relation is to a great 
extent still obscure. In the first place articular rheumatism 
must here be mentioned, the connection of which with chorea 
everybody knows, but which, however, is not interpreted by 
all authors in the same manner. While the French writers 
especially, among them See and Roger, regard rheumatism as 
an almost regular precursor of chorea, in Germany there is 
much diversity of opinion on this point. Several authorities 
(Lebert, Eichhorst, Striimpell) only state that the two affections 
are relatively frequently found together ; others, with Brieger, 
draw attention to the alternating appearance of the two (Ber- 
liner klin. Wochenschrift, 1886, xxiii, 10); again others (He- 
noch, Litten) look upon rheumatism as " the most important and 
best founded cause of chorea" ; still others, in contradistinction 
to the rest, deny the existence of any connection between the 
two affections (Romberg, v. Niemeyer, Prior). However ob- 
scure this association may be, to deny it absolutely would be 
to set facts at defiance. According to our own opinion, we 
have to deal with a common noxious agent, an infection which, 



DIAGNOSIS OF CHOREA. 



477 



if chiefly localized in the brain, gives rise to choreic move- 
ments, while if it affects the joints it causes acute rheumatism 
in them. Most probably, we may almost say unquestionably, 
it is the same infectious material which, if affecting the heart, 
produces endocarditis and myocarditis, for chorea is as fre- 
quently connected with valvular disease of the heart as with 
articular rheumatism, though the one relationship is as obscure 
as the other. 

If chorea, or, we had better say, if certain forms of chorea 
are actually to be traced to an infection, we can not be sur- 
prised if choreic movements are found to appear after other 
infectious diseases — e. g., whooping-cough, typhoid fever, diph- 
theria, or cholera. 

The possibility that chorea has some connection with epi- 
lepsy can not a priori be thrown aside. I have twice had occa- 
sion to observe children who up to the age of puberty had re- 
peatedly suffered, as it seemed, from genuine chorea, and who 
afterward became subject to epileptic attacks. It is true the 
tongue was not bitten in these paroxysms, but otherwise all 
the signs of a classical epilepsy were present, not excluding the 
aura. A later communication of Marie (Progr. med., 1886, xiv, 
page 39), in which the occurrence of ovarian hyperesthesia in 
the course of chorea is mentioned, led us to the idea that pos- 
sibly the above-mentioned attacks were of a hysterical nature 
and to question whether there may not be certain forms of St. 
Vitus' dance which could be designated as hysterical. 

Lastly, those very rare cases of tropho-neurotic disturb- 
ances in chorea are of interest ; thus, bald spots on the skull 
(Escherich, Mitth. aus der med. Klinik zu Wiirzburg, 1886, ii), 
or in places absence of pigment in the hair or the skin, were 
noted (Mobius, Schmidt's Jahrb., 1886, vol. ccix, page 251). 
How these are brought about we are utterly unable to explain. 

Diagnosis. — It is usually not difficult to recognize chorea if 
we remember that young patients of the female sex, who are 
often also anaemic, form the largest contingent of the cases, 
that the twitchings chiefly affect the upper extremities and the 
face, and that they are entirely independent of the will of the 
patient. Their disappearance also during sleep is an important 
point, and this fact by itself would distinguish them from the 
athetoid movements. These latter, possibly the twitchings of 
the tic convulsif, the tremor of paralysis agitans, the shaking 
movements of the intention tremor of multiple sclerosis, finally, 



478 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

certain muscular spasms, which Leclerc and Royer (cf. lit.) 
have designated as pseudo-choreas, must more especially be 
taken into consideration, but they ought never to render the 
diagnosis really difficult. 

Pathology. — Our knowledge of the pathology of idiopathic, 
uncomplicated chorea is very imperfect. Repeatedly capillary 
emboli have been found at the autopsy in the thalamus and the 
corpus striatum, often they could not be demonstrated. The 
experiments of Money on guinea-pigs and dogs (Lancet, 1885, 
1, page 985) would indicate very decidedly that chorea can be 
caused by capillary emboli. Their mode of action, however, 
remains unexplained. The objections which Litten has raised 
against the embolic theory, that the demonstration of embolic 
processes in ordinary cases of chorea is not proved, and that in 
spite of the diversity of the localization of the foci of softening 
in the brain the clinical picture is always the same, can not be 
regarded as convincing. 

The communication of Flechsig, who in the two inner an- 
terior segments of the lenticular nucleus, but nowhere else, 
found small bodies in the lymph sheaths of the vessels, some 
of which were larger, some smaller than blood-corpuscles, has 
since been neither confirmed nor overthrown. " Their arrange- 
ment resembled that of glandular structures ; they were strong- 
ly refractive, very firm, and almost like chalk, although they 
contained no lime. In alkalies they slowly swelled." Though 
their chemical nature is unknown, they resemble in the main 
that material which von Recklinghausen has termed " hya- 
line." This observation has not as yet been interpreted, and 
Flechsig himself declines to give a decided opinion as to 
whether the bodies have been formed in the blood or lymph 
vessels or whether they have to be regarded as products of de- 
generation from ganglionic cells and nerve fibres. Although 
we have to admit that lesions in the lenticular nucleus may 
cause choreic movements, we can as yet make little use of 
these bodies as an anatomical cause for the disease. Earlier 
observations of conditions which were considered as signifi- 
cant for chorea — that is, hyperasmia of the brain and the spinal 
cord, lesions of the corpora quadrigemina, tubercles in the 
cerebellar peduncles, inflammatory conditions in the vertebras, 
and spinal irritation resulting therefrom — possess only histor- 
ical interest. 

Although we are then still unable to say anything definite 



ETIOLOGY OF CHOREA. 



479 



about the nature of the disease, the assumption that we have 
before us an affection of the entire nervous system, in which, to 
be sure, the brain takes the most prominent part, seems the, 
most probable. Whether certain portions of the brain are par- 
ticularly qualified to produce choreic movements — whether, be- 
sides being produced by irritation of the cortical motor centres, 
they may also be brought about by lesions of the basal ganglia ; 
further, whether this irritation can ever be attributed to in- 
fectious material, microbes, or the like, or whether it can ever 
be connected with fungous growths, such as, for example, 
Naunyn has found in the pia belonging to the species of the 
cladothrix or leptothrix — all these remain open questions, and 
we must also leave undecided whether or not perhaps the 
alteration of the blood depending upon the so-called rheumatic 
diathesis is sufficient for the development of the disease. 

^Etiology. — Among the causes of chorea heredity plays an 
important role, as it does in all diseases of the general nervous 
system. This factor is more important, since heredity can here 
not only be called an indirect predisposing circumstance, ow- 
ing to which an individual is more prone to one or the other 
nervous disease, but because there exists actually a hereditary 
form of chorea which is handed down from generation to gen- 
eration and which for a great many years may remain in the 
family. This chorea hereditaria, or, as it is also called, Hunt- 
ington's chorea, does not set in as the common chorea does, in 
childhood, but usually not until the age of thirty or forty. It 
attains the highest degree of those above described, and not 
rarely leads to pronounced mental deterioration. It is incura- 
ble. There are " chorea families " in which a whole generation 
never remains free from the disease and only certain members 
are exempt. On the other hand, there exists also a chorea 
congenita (Rau, Inaug. Dissert., Berlin, 1887), which has to be 
attributed to an affection of the mother caused by fright, etc., 
during pregnancy (Fox, Richter, Mobius, Oppenheim). It has 
long been known that pregnancy itself may to a certain extent 
predispose to chorea, as is shown by the so-called chorea gravi- 
darum. Age and sex play a certain role among predisposing 
causes, inasmuch as the young and the female sex are espe- 
cially prone to it. Among 439 cases, 322 (that is, seventy- 
three per cent) were girls, and 340 (that is, seventy-four per 
cent) were between the ages of five and fifteen; 411 (that is, 
ninety-one per cent) were between the ages of five and twenty 



480 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



(Mackenzie). In rare cases old people become subject to chorea 
(chorea senilis). The oldest of my patients was eighty-one, the 
oldest of Mackenzie's patients even eighty-six. 

Among the exciting causes there are two kinds which are 
particularly important — the one, psychical excitement, particu- 
larly fright and anxiety ; the second, frequent contact with indi- 
viduals suffering from chorea, which awakens an impulse to 
imitate the pathological movements and gives rise to what we 
then call chorea imitatoria. The latter is far less important 
than the former, as the imitation choreas are much more uncom- 
mon than those depending upon psychical emotions. In Mac- 
kenzie's report the cases of chorea caused by fright amounted 
to sixteen per cent, which seems to be a rather large propor- 
tion. The time which elapses between the reception of the 
noxious influence and the development of the disease usually 
comprises from five to seven days, sometimes only one day. 
Sometimes, again, the effect follows the cause immediately, this 
being so in ten per cent of all cases caused by fright. Besides 
fright, bodily or mental overexertion, particularly the latter, 
may become the cause of the disease. According to Macken- 
zie's report, sixteen per cent of all cases observed are attribu- 
table to this cause. 

Treatment. — Cases of uncomplicated chorea get well with- 
out any interference on the part of the physician, but the re- 
sults of wide and varied experience have taught us that with 
certain measures we are able to cut short the duration of the 
disease to a no inconsiderable extent. With reference to the 
internal treatment it is interesting to follow up the different 
phases and changes through which this has passed in the last 
half century. When the spinal cord was supposed to be the 
seat of the disease much was thought of strychnine, which had 
been recommended by Trousseau and which was administered 
in the form of a sirup. Later, when to the rheumatic basis of 
chorea a prominent place was given, colchicum and quinine 
were preferred. Again, camphor, potassium iodide, and hy- 
drocyanic-acid preparations were prescribed when irritation of 
the sexual organs was held to be the starting point of the dis- 
ease. Venesection, leeches, cups to the head and along the 
vertebral column, were applied for a time on the authority of 
Sydenham. All these measures have now more or less fallen 
into oblivion, and even the zincum oxidum album, once so 
warmly recommended by Hufeland, has had to give way to 



TREATMENT OF CHOREA. 48 1 

other remedies. Among those still valued, arsenic, which was 
introduced by Romberg, stands first. It is best given in the 
form of Fowler's solution, in doses of from three to five drops 
three times a day, the dose being gradually increased to twenty 
or thirty drops a day. The medicine ought to be well diluted 
with water. Instead of Fowler's solution we might prescribe 
the waters of the Roncegno or Levico springs in doses of a 
teaspoonful to a tablespoonful three times a day. At the same 
time we must be on the lookout for intoxication, which has 
been known to be produced even by small quantities of the 
drug, as was proved by a case of my own. The arsenic treat- 
ment is to be continued until either the symptoms abate or 
digestive disturbances make their appearance, which would 
contra-indicate its continuance. We usually attain our end in 
from fifty to sixty days. 

Next to arsenic we prefer the salicylate of physostigmine 
(eserine), which, in the form recommended by Riess (Berliner 
klinischer Wochenschrift, 1887, 22), may be injected hypoder- 
mically twice a day in the dose of one milligramme ('/^ gr.). 
Excellent results may be obtained with this mode of treatment, 
and the duration of the disease may be reduced to thirty or 
forty days. We need hardly insist that this drug must be ad- 
ministered most cautiously, because eserine poisoning has been 
observed (Lodderstadt, Berliner klin. Wochenschr., 1888, 17). 
As soon as any bad effects begin to show themselves, such as 
nausea, vomiting, etc., it is advisable to discontinue the medi- 
cine at once for a considerable time. About antipyrine, which 
has been recommended b}' Legroux and others, we can not 
speak so favorably. The results obtained with this drug are 
uncertain and transient. We were never able to note cures 
within from six to twenty-seven days with this remedy, such 
as Legroux has reported. If these medicines leave us in the 
lurch we may with caution prescribe chloral, morphine, opium, 
under the influence of which the movements may temporarily 
abate. 

Among other measures we may mention the use of cold 
water and electricity, which, although only of secondary im- 
portance, may not be without good effects. We have in dif- 
ferent places spoken of the cold-water treatment, and wish 
again to repeat here that extremely low temperatures are un- 
necessary, but rather that hip baths of 84 F., with cold affu- 
sions to the back (8i° to 75 F.) and wet packs seem sufficient. 
31 



482 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

In the electrical treatment chiefly the constant current is to be 
used, which is made to act alternately upon the brain and the 
spinal cord (Erb, loc. cit., p. 587). 

Sometimes all these means of treatment which we have 
just described are ineffectual. The patients take medicine, 
undergo the cold-water treatment, etc., and no improvement 
is noticeable. In such instances a change of climate is to be 
recommended ; the patient may be advised to travel, and be 
kept away from his family for some time ; excitable individ- 
uals especially, in whom psychical influences increase the 
motor irritation, are to be secluded as much as possible. 
Visits of friends or members of the family should be inter- 
dicted. Children should be kept away from school, and should 
be spared any mental exertion. Even at home they should 
not be made to work ; they should be encouraged to suppress 
the movements as much as possible, and a small reward should 
be promised if they succeed. In this manner often a good 
deal is attained. Only in exceptional cases need the patient 
be in bed for any length of time — namely, if the twitchings 
are very violent and likely to lead to bodily injury. In such 
instances the use of narcotics, as suggested above, becomes 
more especially warrantable. 

The symptomatic chorea, or rather the cerebral and spinal 
diseases in which choreiform movements occur as symptoms, we 
need not here describe, as we have already called attention to 
them at the appropriate places. It will hardly ever be difficult 
to decide in a given case the question whether the movements 
before us are due to a functional neurosis — that is, whether the 
case is one of an uncomplicated idiopathic chorea — or second- 
ary only to cerebral or spinal lesions. 

LITERATURE. 

Henoch. Berl. klin. Wochenschr., 1883, 52. 

Vassitch. Etude sur les chorees des adultes. These de Paris, 1883. 

Ferrand. Choree respiratoire. Gaz. med. de Paris. 1884, 41. 

Bokai. Jahrb. f. Kinderheilk., 1884, N. F., xxi, p. 411. 

Peiper. Chorea bei Typh. abdom. Deutsche med. Wochenschr., 1885, 8. 

Holden. Ch. laryngis. New York Med. Journ., January 10, 1885. 

Dickinson. On Chorea, with Reference to its Supposed Origin in Embolism. 

Lancet, January 2, 1886. 
Litten. Beitrage zur Aetiologie der Chorea. Charite-Annal., 1886, xi, p. 265. 
Birnbaum. Ueber die Chorea der Erwachsenen. Inaug. Dissert. Berlin, 1886. 



LITERATURE OF CHOREA. 



483 



Hawkins. Chorea and Epilepsy. Lancet, January 2, 1886. 

Leclerc et Royer. Revue de med., 1887, 2. 

School-made Chorea. Lancet, January 15, 1887. 

Landois. Deutsche med. Wochenschr., 1887, 31. 

Rau. Inaug. Diss. Berlin, 1887. 

Mackenzie. Report on Chorea. Brit. Med. Journ., February 26, 1887. (Re- 
ports of the Collective Investigation Committee of the British Medical As- 
sociation.) 

Koch, P. Zur Lehre von der Ch. minor. Deutsches Arch. f. klin. Med., 1887, 
xl, 5, 6. 

Schwarz. Pester med. -chir. Presse, 1887. 

Schvveinitz. Examination of the Eyes in Fifty Cases of Chorea in Children. 
New York Med. Journ., June 23, 1888. 

Suckling. Brit. Med. Journ., April 28, 1888. (Senile chorea.) 

Comby. Les relations pathog6niques de la choree. Progr. med., 1888, 16, p. 
300. 

Hoffmann. Ueber Ch. chronica progressiva. Virchow's Archiv, 1888, Bd. iii, 
H. 3. (Huntington's chorea.) 

Schromann. Deutsche med. Wochenschr., 1888, xiv, 32. 

Mendel. Centralbl. f. Nervenheilk., 1888, xi, 15. 

Lannois. Ch. hereditaire. Revue de med., 1888, 8. 

Chauvreau. Les tics coordines avec emission brusque et involontaire des cris 
et des mots articules. These de Bordeaux, 1888. 

Herringham. Chronic Hereditary Chorea. Brain, 1888, xi, p. 415. 

Jakowenko. Zur Frage der Localisation der Chorea. Centralbl. f. Nervenheilk., 
1888, xi, 22. 

Klippel et Ducellier. Un cas de choree hereditaire de l'adulte. Encephale, 
1888, viii, 6. 

Patella. Contribuzione anatomo patologica e clinica alia studio della corea mi- 
nore. Padova, 1888. 

Sinkler. Hereditary Chorea. Boston Medical and Surgical Journ., October 15, 
1888, cxix. 

Sturges. The Relation of Chorea to Rheumatism. Lancet, 1889, i, 3. 

Hegge. Ueber den Zusammenhang zwischen Chorea minor mit der Polyar- 
thritis rheum, und der Endocarditis. Wiener med. Blatter, 1888, 41, 42. 

Schadle. Chorea of the Soft Palate. Phila. Med. and Surg. Rep., October 14, 
1888, lix. 

Gairdner. Case of Nerve Disease with Choreic Movements. Glasgow Medical 
Journ., i88q, xxxi, 1. 



CHAPTER II. 

TETANY — TETANILLA TETANUS INTERMITTENS. 

The name tetany (Corvisart) has been given to a neurosis 
which is characterized by paroxysmal tonic muscular spasms, 
during which consciousness remains undisturbed. The spasms 
are often confined to the flexors of the fingers and of the wrist 
joint, and only rarely attack the muscles of the lower extrem- 
ities; they are always bilateral. The fingers are drawn to- 
gether and the hand assumes, to use Trousseau's comparison, 
the shape which the obstetrician gives it when introducing it 
into the vagina. With these spasms, which are of great inten- 
sity, so that the affected muscles feel tense and hard as boards, 
are associated slight flexion at the elbow joint and a moderate 
adduction of the upper arm. Herard claims that the pressure 
of the thumb upon the other fingers may be so strong as to 
lead to pressure gangrene, but this is unquestionably very 
rare. If the lower extremities are affected the feet assume a 
position of plantar flexion, and the big toe is drawn under the 
second or third. Sensory disturbances are usually entirely 
absent, only the contracted muscles are painful on pressure 
and the skin over them is covered with a copious sweat. 

These attacks, which vary a good deal in frequency as well 
as in duration, may be produced by pressure upon the larger 
nerve trunks or the larger arteries of the upper extremities, 
as Trousseau has found accidentally, by applying a venesec- 
tion bandage ; thus, by pressure upon the median nerve or 
the brachial artery, a spasm may be produced of exactly the 
same nature as the spontaneous ones. This is called Trous- 
seau's sign, and is considered to be of great diagnostic im- 
portance. 

The attacks rarely ever occur suddenly and unexpectedly. 
Generally they are preceded by prodromal symptoms, which 
last for a few minutes and consist in a painful drawing sensa- 



TETANY. 



485 



tion in the hands and arms. Previous to the first attack such 
sensations, together with formication, feelings of coldness, etc., 
may have existed for weeks. The attacks last rarely more 
than five or ten, usually they are over in one or two, minutes, 
and it is only in exceptional instances that they go on for sev- 
eral hours. Their frequency also varies as we have said. 
Some patients — just as now and then happens in epilepsy — 
have not more than one all their life, some have several a 
day, and in others again weeks, months, or years pass between 
the individual attacks, and the whole disease may extend over 
twenty or thirty years. . In all cases, however, provided there 
exist no complications — such as joint affections — the outcome 
is favorable, and in no case can any lasting bad effects upon the 
organism in general be noticed. In the intervals the patient 
does not complain of anything and feels in perfect health. 
Only an objective sign is demonstrable, which betrays that 
everything is not going on normally— namely, an increase, not 
only of the electrical, but also of the mechanical excitability of 
the nerves — a condition to which Erb has called attention. 
Even a weak current produces a marked effect, and by simply 
stroking the face with the finger it is possible to elicit lively 
contractions of the muscles supplied by the facial nerve. Al- 
though this sign is not constant, since it has in cases of tetany 
been looked for in vain, even after the most careful examina- 
tions, and although we must not forget that it occurs not in 
tetany alone, but also in organic diseases of the spinal cord — 
e. g., in glioma — it remains, nevertheless, very valuable, and 
must certainly be taken into account in the diagnosis. 

The anatomical seat of the disease is still obscure. It has 
been referred to the most varied parts of the nervous system, 
to the cerebrum, the cerebellum, the spinal cord, the periph- 
eral nerves, even to the sympathetic, which seems anyhow to 
be the part of the nervous system which is blamed for affec- 
tions we can not locate. All these, one after the other, have 
been suspected of playing a role in the pathogenesis of tetany, 
but proofs have never been brought forward for the correct- 
ness of any of these views. 

The least probable theory seems to be the one which as- 
sumes the disease to be of a peripheral nature. This can hardly 
be brought into accord with the fact that the affection has been 
known to follow psychical influences, for, just as we have seen 
to be the case in chorea, and as we shall soon learn for epi- 



486 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

lepsy, so this disease can be brought about by imitation, and 
indeed there have been instances recorded where in this man- 
ner even small epidemics of tetany appeared in schools (Mag- 
nan, Gaz. de Paris, 1876, 50, and Gaz. des hop., 1876, 141). 
The disease has further been observed in women who are suck- 
ling infants, in young mothers and wet nurses ; and so fre- 
quently has this been the case that Trousseau felt himself jus- 
tified in terming tetany " la contracture des nourrices." Quite 
inexplicable are those cases occurring after extirpation of 
goitres (N. Weiss, Falkson, and others) and after infectious dis- 
eases, especially scarlet and typhoid fevers. All this speaks, 
however, in favor of the central nature of the disease, as does 
also the fact that the occupation may have some causative in- 
fluence, inasmuch as people who have to use their arms, hands, 
and fingers a great deal — telegraph operators, seamstresses 
(Mader, Hirt) — are relatively frequently subject to it. Ac- 
cording to our opinion, the cortical nature of tetany is as prob- 
able as the cortical nature of writer's cramp. 

The great rarity with which the affection occurs makes it 
practically of little importance. If we add to this that the 
cases, which we see, run without exception a favorable course, 
one can understand why but little is to be said of the treatment. 
If any interference be necessary or desirable we may avail our- 
selves of the galvanic current, placing the anode over the af- 
fected parts and the cathode • in some indifferent place. This 
may be repeated two or three times a week, each time a mod- 
erate current being allowed to pass for from three to five min- 
utes. During the attack this procedure is sometimes quite 
beneficial, whereas upon the course of the disease it has as little 
influence as the well-known nervines. We have used tepid 
baths with success, inasmuch as the patients felt very comfort- 
able in them and claimed to be able to notice a diminution in 
the frequency of the attacks. It is our opinion, however, that 
even the baths can be dispensed with and that it is best not to 
subject the patient to any therapeutic measures at all. 

LITERATURE. 

Schultze, Fr. Ueber Tetanie und die mechanische Erregbarkeit der peripheren 
Nervenstamme. Deutsche med. Wochenschr., 1882, 20, 21. 

Mader. Ueber die Beziehung der Beschaftigungskrampfe zur Tetanie. Wiener 
med. Blatter, 1883, 16. 

Lederer. Jahrb. f. Kinderheilk., 1883, xxii, 4. 



THOM SEX'S DISEASE. 



487 



Baginsky. Tetanie bei Sauglingen. Archiv f. Kinderheilk., 1886, vii, 5. 

Meinert. Archiv f. Gyn., 1887, xxx, 3. 

Schotten. Berl. klin. Wochenschr., 1888, xxv, 14. 

Hoffmann (Heidelberg). Zur Lehre von der Tetanie. Deutsches Archiv f. 

klin. Med., 1888, xliii, 1. 
Frankl-Hochwart v. Ueber mechanische und elektrische Erregbarkeit der 

Nerven und Muskeln bei Tetanie. Ibid., 1888, xliii, 1. 

Thomsen's Disease. — Under the name of Thomsen's disease 
an affection has been described which is characterized by " tonic 
spasms in the muscles during voluntary movements." When any 
muscle is moved voluntarily, as it contracts, a tonic, painless spasm 
comes on which either greatly impedes the intended movement or 
completely frustrates it. If the patient wishes to perform certain 
motions a sensation of fatigue is felt in the part and a resistance, 
which he has first to overcome before the intended movement can be 
executed. Objects which he is holding in his hands he can not let 
go at once and put down. Running, dancing, gymnastics, the ma- 
nipulations of the military drill, are absolutely impossible, and any 
such attempts distress him very much and bring him into the most 
annoying situations. If the musculature of the tongue is implicated 
a motor speech disturbance is added. Sensory disorders are not 
found, and in general the patients are perfectly well if they do not 
attempt to move. Objectively may be noted, besides the increased 
excitability to the galvanic current, an unusually strong development 
of the musculature and an increased power which seem almost to 
belie the complaints of the patients that they are embarrassed in 
their movements. 

Heredity stands for a great deal in the disease, which was evi- 
dent from the first from the description which Thomsen himself gave 
in 1876. He reported that in his own family in five generations 
more than twenty persons had suffered from it. Often it is con- 
genital, hence Strumpell has proposed the name myotonia con- 
genita. 

The nature of the malady is still a matter of conjecture. The 
fact that on galvanic stimulation of the muscles the contractures are 
slow and very prolonged, lasting even as much as thirty seconds — 
myotonic reaction of Erb — the observation of Erb that on micro- 
scopical examination the muscular fibres are seen to be broader, the 
nuclei multiplied, and the interstitial connective tissue increased, are 
not points sufficient to warrant a definite decision about the seat of 
the disease Still, the possibility that we are actually dealing with 
an affection of the muscles is by no means excluded. 

The disease, which interferes greatly with the occupation, is wont 
to last throughout the entire life. The patients learn to accommo- 



4 88 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

date themselves to a certain extent to the inconvenience, and by 
allowing for it are able in a measure to hide their awkwardness. In 
countries where military service is compulsory any one suffering 
from myotonia is exempt. No treatment has as yet been promul- 
gated for this rarest of affections. 

LITERATURE. 

Thomsen (in Kappeln). Tonische Krampfe in willkurlich bewegten Muskeln. 

Arch. f. Psych, und Nervenkrankheiten, 1876, vi, 3. 
Seeligmiiller. Deutsche med. Wochenschr., 1876, ii. 
Bernhardt. Virchow's Archiv, 1879, lxxv. 
Peters. Deutsche militararztl. Zeitg., 1879, viii. 
Striimpell. Berl. klin. Wochenschr., 1881, xviii, 9. 
Ballet et Marie. Arch, de neurologie, 1883, v, 13. 
Westphal. Berl. klin. Wochenschr., 1883, xx, No. 20. 
Weichmann. Ueber Myotonia intermittens congenita. Dissert, inaugur. 

Vratisl., 1883. 
Mobius. Schmidt's Jahrbiicher, 1883, Bd. cxcviii, p. 236. 
Rieder. Deutsche militararztl. Zeitg., 1884, xiii. 
Pitres et Dallidet. Arch, de neurol., 1885, x. 
Eulenburg und Melchert. Berl. klin. Wochenschr., 1885, xxii, 38. 
Erb. Die Thomsen'sche Krankheit. Leipzig, Vogel, 1886. 
Fischer. Neurol. Centralbl., 1886, v, 4. 
Eichhorst. Handb. etc., 1887, 3. Aufl., p. 307. 
Striimpell. Lehrb. etc., 1887, 4. Aufl., p. 463. 
Buzzard. Lancet, May 14, 1887, i, 20. 
Jacoby. Journ. of Nerv. and Ment. Dis., 1887, xiv, 3. 
Blumenau. Ueber die elektrische Reaction der Muskeln bei der Thomsen'schen 

Krankheit. Centralbl. f. Nervenheilk., 1888, xi, 22. 
Dana. Thomsen's Disease. Journ. of Nerv. and Ment. Diseases, April 4, 1888, 

N. S., xiii, 



CHAPTER III. 

PARALYSIS AGITANS — SHAKING PALSY — PARKINSON'S DISEASE — 
CHOREA PROCURSIVA. 

Among the diseases of which we are treating in this part 
paralysis agitans is the gravest, but happily also the rarest, for, 
according to statistics of my own cases, only about 0.43 per 
cent, or one in two hundred and twenty-nine, of all affections 
of the nervous system were instances of paralysis agitans. 
Within the some sixty years which have passed since Parkin- 
son's description appeared, certain symptoms of the disease 
have, it is true, been studied more carefully, but our knowl- 
edge of the aetiology, the anatomical seat, the treatment, etc., 
has not improved to any extent, and in fact our progress has 
been unsatisfactory. 

Symptoms. — The first thing observed by the patient is a 
feeling of weakness in the extremities, followed soon after by a 
slight tremor, which at first only occurs temporarily. It is 
more marked in the upper extremities, especially in the right 
arm, yet it is also noticeable in the legs, and exceptionally in 
the head. The old idea that the head is always exempt from 
the tremor of paralysis agitans, and that this exemption is, 
cceteris paribus, characteristic of the affection, is untenable. In 
rare instances the tremor is confined to one half of the body, 
whereas the other remains quiet. 

The tremor consists of uniform oscillating movements, the 
oscillations being rather few in number, not more than from 
four and three quarters to five and a half per second (Cramer), 
whereas the tremor of Graves's disease, for example, presents 
from nine to nine and a half oscillations per second (Marie). 
The lengths of the oscillation waves have been studied by Marie, 
Cramer, and others, and the handwriting of the patients has gen- 
erally been utilized for such observations. The oscillations were 
recorded on paper by means of a Marey's drum or rubber ball, 



49Q 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



which the patient was made to hold loosely in his hand. Re- 
peatedly with perfect regularity of the wave lengths a varia- 
bility in their height could be demonstrated, the physiological 
cause for which is not entirely clear. It is not infrequently 
seen that the tremor increases on forced attempts at motion, 
and passes into a regular " shake," so that the patient, although 
not entirely helpless, becomes very awkward in feeding himself. 
It is a fact of considerable diagnostic importance that the 




&#■ 





*~7C^7 



^4.oi^l/f.%, 



<7 



*?. 




[57.— Specimen of Handwriting of Patient with Paralysis Agitans (personal 
observation). 



movements during rest in bed do not cease, but continue and 
hinder the patient from getting to sleep, and (in contradistinc- 
tion to what we find in chorea) do not disappear even during 
sound slumber. Indeed, the intensity of the tremor may remain 
undiminished in bed, and I know of instances in which the pa- 
tients procured for themselves iron bedsteads in order to avoid 
the annoying creaking of the wooden bed caused by the vio- 
lent shaking. In other cases the condition improved upon 
lying quietly in bed, and falling asleep was facilitated by the 
use of certain artifices. Thus Eichhorst relates of one of his 
patients that he always carried a little twig between his teeth 
so as to keep his jaws quiet, and one of my own cases only 



PARALYSIS AGITANS. 4 n r 

could obtain comfort and a certain amount of rest in his fingers 
and arms by rolling small objects — for instance, little wooden 
balls which he had made for the purpose — between his fingers 
and thumb. With the aid of these he also could go to sleep. 
If by accident he left these balls at home, he unconsciously 
picked up other objects which might be lying before him, such 
as matches, or he rolled bread pellets, and so on, and only felt 
comfortable when his fingers were occupied with something of 
this sort. The change in the handwriting caused by this 
tremor is illustrated in Figs. 157 and 158. 

In connection with, and probably as a consequence of, the 
trembling movements, gradually a condition develops in which 

Fig. 158.— Specimen of Handwriting of Patient with Paralysis Agitans (personal 
observation). 

the patient gets easily tired, the muscular strength diminishes, 
and the muscles assume a certain rigidity which influences the 
position of the body and the extremities when at rest as well 
as on voluntary motion. The position of the body is charac- 
teristic. Not only the head, which affords a good deal of re- 
sistance to passive movements, but also the whole trunk is 
somewhat bent over, and it appears as if the patient was at 
every moment ready to fall forward. The arms, which are 
bent at the elbows, are in close apposition to the trunk, the 
thumb rests against the fingers, so that the hand assumes some 
such position as it would in writing, the fingers themselves 
being flexed in the metacarpal joints (Fig. 159). The knees 
are so close together that the trousers are rubbed against each 
other by the trembling movements, and walking is not a little 
interfered with. The legs are usually slightly flexed at the 
knee joints, while nothing remarkable can be noticed about 
the joints of the toes. The patient impresses one as being in 
a constant state of uncertainty and perplexity, an impression 
which is only diminished to a certain degree by the very char- 



492 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



acteristic facies. The rigidity being also marked in the mus- 
cles supplied by the seventh nerve, the face has an expression 
of majestic calm, nay, even of sublimity. The patient seems 
inaccessible to psychical emotions. His smile is hardly per- 
ceptible, since the lower portions of the face more especially 
are almost immobile. Only the wrinkling of the forehead is 
somewhat more marked. Sometimes the patients have a 
peculiar piping voice, such as an actor assumes when playing 
the part of an old man on the stage. 

We have already alluded to the fact that voluntary move- 
ments are somewhat impeded. This is not only due to the 
tremor, but also to the already-mentioned general weakness. 




Fig. 159.— Position of Hands and Fingers in Paralysis Agitans (as if holding a 
pen). (After Eichiiorst.) 

He is, therefore, helpless, and needs some one to assist him if 
he wishes to sit up in bed or even to change his position. If 
he is in a sitting posture rising is difficult, sometimes impos- 
sible. The act of walking is not normally performed, for be- 
sides the bent position, which in walking becomes even more 
exaggerated than in standing, the patient once started has an 
irresistible tendency, owing to the displacement of his centre of 
gravity forward, to hurry ahead ; his steps, at first short and 
tripping, become quicker and longer, and so great may be the 
force with which he involuntarily rushes forward that if there 
is no one there to stop him he falls on his face with great vio- 



PARALYSIS AGITANS. 493 

lence. The same phenomenon, which is called "propulsion," 
may sometimes be artificially produced by pulling the patient 
forward by the coat while he is walking quietly. He then 
goes faster and faster, and finally breaks into a run alarming to 
the bystanders. Much more rarely do we find a similar con- 
dition in the backward motion (" retropulsion "), so that the 




Fig, 160.— Position of the Body in Paralysis Agitans (personal observation). 

patient if pulled from behind walks backward faster and faster, 
to fall over in a short time. Charcot looks upon these phe- 
nomena as forced movements, a view which has, however, 
never been substantiated. They may possibly be explained on 
purely physical grounds as being due to the displacement of 
the centre of gravity of the body (Striimpell). 

Trophic changes, with the exception perhaps of the tran- 
sient appearance of purpuric spots symmetrically on the arms 
and legs ("senile purpura "), are not met with. Changes in 
the electrical excitability of the muscles do not occur, or are, 
at any rate, not the rule. Sensation and reflexes remain entirely 



494 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



normal, and bladder as well as rectal symptoms are not pres- 
ent. An increase in the body temperature can never be dem- 
onstrated objectively, although patients complain at times of 
subjective feelings of increased heat and a disagreeable tend- 
ency to sweat a good deal, which is especially pronounced 
when lying in bed, so that they often sleep uncovered or with 
but little over them. If any cerebral or spinal symptoms make 
their appearance these have to be regarded as complications. 
They do not belong to the clinical picture of paralysis agitans 
as we know it now. 

Cases in which muscular weakness and rigidity, with all 
their inconvenient consequences, were present, in which, also, 
the so-called propulsion was marked, but the tremor was ab- 
sent, have been reported (Amidon, New York Medical Record, 
1883, xxiv, 21), but such are rare. 

The nature of the disease is not yet understood. We do 
not even know whether to refer it to the brain or to the mus- 
cles. Much less, of course, do we know where the exact seat 
should be sought for in the nervous system. Before the labors 
of Charcot and Ordenstein, paralysis agitans was often con- 
founded with multiple sclerosis, and various anatomical lesions 
were then described as underlying the paralysis agitans. Later 
the error was cleared up, and even to the present day we are 
not acquainted with any anatomical basis for the disease. 

^Etiology. — Uncertain is our knowledge also about the 
causes. Of course here, as in all other nervous diseases, hered- 
ity and the importance of a neuropathic family history must 
be spoken of, yet the rarity with which the affection occurs 
shows that this factor alone is seldom sufficient to cause the 
disease. Hence other exciting causes must come into play, 
but it is a fact difficult to understand why the same factors 
which so often give rise to chorea so rarely produce a shaking 
palsy. The causes for all these diseases are always the same, 
or at least similar, and it is here also in the first place that 
psychical emotions of fright and anxiety are of moment. The 
French physicians have at no time seen develop so many cases 
of paralysis agitans as during the time of the siege in 1871, and 
for years after the relative frequency of the trouble in the Paris 
hospitals, particularly in the Salpetriere, acted as reminders of 
the terrible hours which the besieged must have gone through. 
In private practice we also have occasion to find that psychical 
causes bring about the disease ; more frequently, however, at 



PARALYSIS AGITANS. 495 

least in my own experience, no cause at all can be found. The 
influence of exposure to cold and of overexertion of course has 
here also been thought to be of astiological significance without 
there being any grounds for such an assumption ; on the other 
hand, there is no question but that certain infectious diseases — 
e. g., intermittent fever, pertussis, typhoid fever — may be fol- 
lowed by a paralysis agitans, a connection, however, which, 
although certain in its existence, is still obscure in its nature. 
Nothing definite is known about the influence of age and sex. 

Diagnosis. — After what has been said little needs to be 
added with regard to the diagnosis, which is almost always 
easy. It is certainly not hard to avoid mistaking paralysis 
agitans for multiple sclerosis or chorea, and chronic alcoholism 
is easily excluded if we take into account the characteristics of 
the tremor, its continuance during sleep, and the whole course 
of the disease. It may be sometimes difficult to differentiate a 
shaking palsy from the ordinary tremor senilis if the latter 
occurs as early as the forties, at a time of life during which 
paralysis agitans is not rare, and it is the more necessary to be 
careful since the number of the oscillations in both affections 
is about the same, that is, ranges between four and six per 
second. The muscular weakness, the peculiar rigidity which 
accompanies the movements, the characteristic facial expres- 
sion, the posture, the " propulsion," etc., will in most cases be 
sufficient to clear up the diagnosis. 

Treatment. — The treatment is entirely fruitless. We have 
not as yet seen any results from any of the therapeutic meas- 
ures employed. Neither with baths nor with massage (Ber- 
bez, cf. lit.) nor with galvanism has anything been achieved, 
and all internal medicines are of no avail. It is impossible to 
give particular indications for the treatment, and it must there- 
fore remain for the physician in every case to treat alternately 
with baths, massage, and electricity, according as he sees fit. 
As long as he does not do the patient any harm it does not 
matter much which mode of treatment he decides to use. 
Lately Erb has recommended the muriate of hyoscine injected 
subcutaneously or taken internally. This is said to have a 
very good effect upon the tremor, but whether this effect is 
lasting, and whether the bad after-effects which occasionally 
appear after a prolonged use of the drug are not a grave ob- 
jection to its administration, is not as yet decided. My own 
experiences with it were not favorable. 



496 DISEASES OF THE GENERAL NERVOUS SYSTEM. 



LITERATURE. 

Grashey. Archiv f. Psych, und Nervenkrankh., 1885, xvi, 3, p. 857. 

Riess, L. Beil. klin. Wochenschr., 1887, xxiv, 22. (Recommends the eserine 
treatment.) 

Miiller, Fr. Charite-Annalen, 1887, xii, p. 267. (Implication of the laryngeal 
muscles.) 

Erb. Ueber Hyoscin. Therapeut. Monatsh., Juli 1887. 

Berbez, P., et Berbez, H. Bull, de la Soc. de therap., 1887, xviii, 18. (Recom- 
mend methodical massage.) 

Heimann. Ueber Paralysis agitans. Berlin, Hirschwald, 1888. 

Lacoste. Contribution a l'etude de la maladie de Parkinson. These de Paris, 
1887. (De quelques formes anormales.) 

Huber. Myographische Studien bei Paral. agit. Virchow's Arch., 1887, 108, 1, 

p. 45- 
Teissier. Pathogenie de la paralysie agitans. Lyon med., 1888, lviii, 28. 
Weber. Paralysis Agitans, with Cases. Journ. of Nerv. and Ment. Diseases, 

July 7, 1888, N. S., xiii. 



SECOND GROUP. 

NEUROSES IN WHICH THE ENTIRE ORGANISM IS MORE OR 
LESS SEVERELY IMPLICATED. 



CHAPTER I. 

NEURASTHENIA — NERVOUS PROSTRATION. 

Neurasthenia (a, privative ; crdevos, force) or nervous ex- 
haustion is an affection of the nervous system with which the 
general practitioner meets very frequently, and is one of those 
diseases which may give rise to a good deal of error in diag- 
nosis and prognosis. At the same time it makes the most 
boundless demands upon the forbearance of the physician and 
upon the patience of the sufferer. The disease is a child of the 
modern mode of living, of the desire to become rich as soon as 
possible, and we look for it in vain in the old text-books. Al- 
though it may in earlier times have occurred now and then, 
the neurologists had neither opportunity nor occasion enough 
to study it intimately. This has only become possible quite 
recently, and it is certainly a fact of significance that neuras- 
thenia has been " discovered " in that continent, the inhabit- 
ants of which have the reputation of working the quickest, 
of living at the highest pressure, and therefore of being — of 
course with exceptions — more nervous and aging sooner than 
those of the Old World, to wit, in America. Beard, to whom 
we owe so many excellent observations, so many splendid 
hints for therapeutics, described it first and gave it the name it 
bears. Whereas the disease prior to Beard's publication was 
unknown, it soon began to prevail in such a striking manner 
and to be diagnosticated so frequently that one is almost led 
to think that this diagnosis is often arrived at in cases where 
something else exists, some organic affection possibly more 
difficult to recognize. The disease in question is not organic 
32 



498 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

and not associated with any demonstrable anatomical altera- 
tions. Nobody has ever succeeded in finding- any character- 
istic anatomical changes in individuals who have suffered for 
years from the most pronounced neurasthenic manifestations 
and then have died from some intercurrent disease. A large 
number of subjective complaints, many of which fit into other 
clinical pictures, make it intelligible why a diagnosis of neuras- 
thenia is often made, sometimes without any sufficient, careful, 
consideration of all the factors which ought to be taken into 
account. It is comfortable and presumes nothing. Its possi- 
ble incorrectness can frequently not be demonstrated, and it 
therefore rapidly attained a great popularity among physicians. 
Symptoms. — The first traces of the disease develop very 
gradually and imperceptibly. Sometimes they assume more 
of a cerebral, sometimes more of a spinal character, so that it 
has been thought justifiable to distinguish a spinal and a cere- 
bral neurasthenia. For the cases in which the symptoms of 
derangement of digestion were most prominent the term gas- 
tric neurasthenia was coined, under which head we may possi- 
bly class certain of the so-called nervous dyspepsias. In the 
majority of cases the patients complain of getting easily and 
rapidly fatigued after the bodily exertion which is associated 
with their ordinary daily doings, whether at home or in their 
business, after walks, gymnastic exercise, etc. Things which 
they used to do without the least difficulty tire them greatly. 
In going distances which were formerly covered with ease they 
have to rest half way, and require more time to accomplish a 
given task. Not always are definite pains present. At times 
there are aches in the back and loins severe enough to be 
troublesome. Sensory disturbances, paresthesias, .formication 
in the extremities, or numbness, are rarely absent. I These feel- 
ings distress the patient and may make him fear he has tabes, 
and the idea that he is suffering from some spinal trouble is 
fostered by the circumstance that the sexual power is usually 
decidedly diminished, be it that the patient is unable to have 
connection as often as before, be it that the erection of the 
penis is incomplete or that no ejaculation of semen occurs. 
For married patients this weakness is a source of great distress 
and often is a very prominent symptom, and frequently it is 
this that finally decides them to consult a physician, a step which 
has been again and again deferred. The more we have to deal 
with neurasthenias the more frequently shall we make the ob- 



NEURASTHENIA. 400 

servation that the sexual functions are in the majority of cases 
in some way or other affected, and that the sexual neurasthenia 
particularly deserves the most careful attention of the physi- 
cian. To determine whether the complaints of a patient with 
regard to his disordered sexual functions depend upon organic 
disease or upon neurasthenia we have, besides a careful exam- 
ination of the genitals, to examine the urine. It is well known 
that the urine of neurasthenics not rarely presents a decided 
increase of urates, oxalates, and phosphates, and that not infre- 
quently spermatic fluid is passed during micturition or during 
defecation (Beard and Rockwell, cf. lit.). Where the patients 
complain, as they so commonly do, of impotence, we shall 
have to determine what form we are dealing with, and whether 
organic disease, more particularly atrophy of the testicles, is 
the underlying cause. Sometimes there exists only a decrease 
in the sexual desire, while the power remains the same ; some- 
times a decrease in the power and an increase in the desire, so 
that the ejaculation of semen occurs too early, sometimes be- 
fore the insertion of the penis. Again, both sexual desire and 
power diminish pari passu, or finally the potcntia coeundi is nor- 
mal but there is absence of spermatozoa (" aspermatism "). 

All changes of this kind are noticed by the patient and 
their significance is ever exaggerated by a fervid imagination. 
Even in the cases in which in reality there is no disease and in 
which the impotence depends entirely upon psychical influ- 
ences, it makes itself disagreeably felt, and we must not forget 
that such a " psychical " impotence, in spite of all encouragement 
and all assurances on the part of the physician is sometimes 
more difficult to cure than one which depends upon organic 
disease of the sexual apparatus. Every abortive attempt at 
coitus exerts a depressing influence upon the patient for a con- 
siderable time and is quite liable to lead to a second failure, 
although all other conditions for the normal performance of 
the act may be favorable (Fiirbringer, cf. lit.). \ 

The disturbances of the cerebral functions which appear in 
the course of neurasthenia are very manifold. First, the pa- 
tient is down-hearted and worried and sees everything in the 
blackest colors, and, above all, despairs of recovery. He be- 
comes irritable and impatient, unsociable with his friends, and 
feared by his family. In his work he is less efficient. Duties 
which he previously performed without trouble seem hard to 
him and require twice or three times as long for their accom- 



tjOO DISEASES OF THE GENERAL NERVOUS SYSTEM. 

plishment. Cases in which this is not a prominent feature, but 
where the working power remains unchanged, are met with, 
but are exceptions. The sleep is usually disturbed ; some- 
times a protracted insomnia adds to the trouble. Headache is 
not the rule, but the patient often complains of a disagreeable 
pressure in his head, which is accompanied with a slight feel- 
ing of dizziness. All functions share in the disorder, the appe- 
tite becomes bad, the bowels sluggish, the action of the heart 
feeble, and vaso-motor disturbances in the form of persistent 
coldness of the hands and feet manifest themselves. The gen- 
eral condition of the patient is very pitiable in the higher 
grades of neurasthenia, and it is necessary for the physician 
to make a most careful examination so as not to go astray in 
the diagnosis. 

The objective examination, in contradistinction to what the 
manifold complaints of the patient might lead us to expect, re- 
veals strikingly little. Organic changes can not be demon- 
strated anywhere. Thoracic and abdominal organs are healthy ; 
nothing abnormal can be detected in the domain of the cranial 
nerves or in the fundi of the eyes. The condition of the pupils 
varies. Transient differences in their size — that is, unilateral 
dilatation, without, however, any abnormity in the pupillary 
reflex — is certainly met with. The dilatation may either al- 
ways be on the same side or change at times to the other eye. 
The phenomenon is usually marked when the general condition 
is bad, while it disappears if decided and lasting improvement 
is once established. The claim that lasting inequality of the 
pupils is always a sign of organic disease, as Beard thinks, must 
certainly be somewhat modified (Pelizaeus). I have myself 
seen differences in the pupils persist for eight or ten months 
and then disappear and the patient get well. 

The peripheral nerves as well as the tendon and skin re- 
flexes are normal. Tenderness over the vertebrae rarely is ab- 
sent, but is of no significance. 

Diagnosis. — When we have once sufficiently informed our- 
selves about these points the diagnosis will usually present but 
little difficulty. At first, it is true, we may be easily led astray 
and think of organic diseases of the brain, especially pro- 
gressive paralysis of the insane or a brain tumor, yet the fur- 
ther course of the disease will soon clear the matter up. The 
suspicion of tabes which may arise on account of the cerebral 
and particularly of the spinal symptoms, the disturbances of 



NE URA S THENIA . 5 Q l 

the sexual functions, and so forth, will be discarded, owing to 
the persistence of the patellar reflexes, the absence of actual 
bladder symptoms and pronounced sensory disturbances, an- 
aesthesias and hyperesthesias, as well as of actual motor weak- 
ness. Fibrillary twitchings, such as are observed in progress- 
ive muscular atrophy, may here also be met with, but they 
are seen rarely and their occurrence varies a good deal. From 
hysteria neurasthenia is distinguished by the fact that the con- 
stant change of the symptoms which is so characteristic of hys- 
teria, besides the circumscribed neuralgias, the contractures, 
the spasms, etc., is here not observed. Still, to make a diag- 
nosis, repeated and careful examinations are needed, to which 
the patients do not submit as willingly as hysterical men and 
women. 

Etiology. — In every case in which hereditary influences 
can be excluded the prime cause of neurasthenia is unques- 
tionably to be looked for in an overtax of the nervous sys- 
tem. This is brought about in many ways, by excessive men- 
tal work or by habitual bodily overexertion. It may be at- 
tributable to repeated emotions or to sexual excesses. Under 
the latter head we may put masturbation,! which is a wide- 
spread evil among the young of both sexes and the practice of 
which not only may begin very early, but may be continued 
much longer than the physician himself might suspect. One 
may say that there are but few neurasthenics who have not 
during their youth been addicted to this habit for a longer or 
shorter period of time. " Sexual perversion " (Spitzka) and 
the various kinds of " psychical masturbation " may also be- 
come of ^etiological significance. Even in married life, where 
the satisfaction of the sexual desire is otherwise well regulated, 
the coitus interruptus sive reservatus, which is practiced to 
avoid too great an increase in the family, may afford a cause 
for neurasthenia. In my experience very few men have been 
able to practice with impunity for years this coitus interruptus, 
and it is the bounden duty of the physician to inquire with 
much tact but still with perseverance into this question. | 

In some cases the abuse of tobacco may lead to neuras- 
thenia, so that the latter has to be looked upon directly as a 
nicotine poisoning, and must, of course, be treated accordingly. 
Persons whose occupation necessitates work not only energetic, 
but also associated with the emotions (artists, students, finan- 
ciers, speculators, etc.), also those whose occupation entails at 



502 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



the same time bodily as well as mental strain, are all more or 
less neurasthenics. Not rarely repeated losses of a consid- 
erable quantity of blood produce neurasthenia by causing a 
general anaemia, yet we must definitely state that the neuras- 
thenia may occur very well in such cases without the anaemia. 
Traumatism also may cause neurasthenic conditions. About 
these, which are usually intermediate forms between this dis- 
ease and hysteria, we shall have to speak later, under the head 
of " traumatic neuroses." Finally, neurasthenia has been known 
to occur after infectious diseases, typhoid fever, cholera, vari- 
ola. In these cases the bad state of nutrition and the faulty 
condition of the blood have to be held responsible. 

Treatment. — The treatment of neurasthenia is one of the 
most troublesome tasks which the physician encounters. It is, 
of course, not sufficient to give the patient a prescription and 
let him go. We must frequently examine him, not only on our 
own account, but for his own sake as well, because he is com- 
forted by the attention and solicitude of the physician, although 
the examination itself is usually disagreeable to him. There are 
neurasthenics who are actually relieved by repeated examina- 
tions, although nothing is ever prescribed. They gain there- 
from the quieting conviction that somebody is looking out for 
them, and this gives them hope. But here also the direct 
psychical treatment, such as we usually find to be of value 
in hysteria, is of the greatest importance. The patient must 
again and again be encouraged and told that all his organs are 
healthy, that it is only a nervous overstrain which he is suffer- 
ing from, a deficit in his nerve capital which it is somewhat 
difficult to replace. To exert a mental influence upon the pa- 
tient in this manner time is necessary, and those physicians who 
can not afford sufficient time for the purpose should not take 
charge of a grave case of neurasthenia at all. 

If hypochondriacal notions are prominent features, so that 
the patient is beyond the reach of consoling and encouraging 
words, the question whether or not he should be removed to 
an institution must come under consideration. In addition to 
the fact that change of air and scene exerts in itself a favorable 
influence, it is advisable to place a neurasthenic after a certain 
time among different surroundings, so that he has to meet with 
different people and has something fresh to occupy his mind 
with, and care should be taken to keep him constantly under 
the guidance of a physician. As supplying such requirements 



NE URA S THEN I A . 



503 



sanitaria for nervous people, in which insane cases are not ad- 
mitted, are to be highly recommended. Of course the pecu- 
niary condition of the family must, before deciding upon this, 
be taken into account, since all establishments of this kind in 
which patients are well cared for are rather expensive. Some- 
times in the more favorable instances a stay of from four to six 
months is sufficient to bring about a very decided improve- 
ment, in which case even families who are not very well off 
should be able to afford the expense. 

There are especially two factors from which much is to be 
expected in the treatment of neurasthenia, and these are elec- 
tricity and hydrotherapy, particularly the cold-water treat- 
ment. With regard to the former it may well be stated that 
there is no other nervous affection in which its application is 
followed by such excellent results as here. Used at the proper 
time and in proper doses, so to speak, it is most beneficial. 
The method which is best employed and to which we give by 
far the preference is the so-called general faradization as rec- 
ommended by Beard and Rockwell, as well as the general gal- 
vanization. The results are especially striking if we make use 
of the brush, which, in Beard's method, is not only applied to 
the back — although it is kept here longest — but (with the ex- 
ception of the head) all over the body. Although the patient 
may complain of disagreeable and painful sensations for the 
five or eight minutes during which the sitting lasts, the after 
effects which soon follow are most gratifying. The patients 
feel invigorated and leave the physician with a sense of having 
gained a new lease of life. According to our experience the 
faradization as advised by Beard is superior in its action to the 
electrical baths, which are much more circumstantial and have 
not been as yet sufficiently studied. 

With reference to the cold-water treatment, to which we 
have repeatedly called attention in different places, we must in 
this more than in any other affection warn against overzeal- 
ousness and insist upon caution. Low temperatures are borne 
very badly by these nervous and irritable patients. They be- 
come excited and sleepless, and our aim is not only frustrated, 
but actually more harm than good is done. However, if we 
cautiously begin with a temperature of from 86° to 78 F., and 
confine our measures to gentle rubbings, affusions of short 
duration, cool hip baths, also of short duration, and avoid 
douches altogether, if care is taken at the same time to insure 



504 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



proper nourishment and exercise for the patient, the best form 
of which, perhaps, is a walk in the woods, the results are en- 
couraging and lasting, if neither physician nor client lose their 
patience too soon. A course of treatment of this kind can not, 
however, be compressed into the usual four weeks of a summer 
vacation, but to do any good six, eight, or ten weeks should be 
taken. Sometimes sea baths will be more useful than the 
simple cold-water treatment, but then also care must be taken 
in their selection. For the excitable and nervous who suffer 
from insomnia the places on the Baltic will on the whole be 
preferable to those on the North Sea, while the latter are 
especially adapted for very prostrated patients and individuals 
suffering from cerebral anaemia. 

A long stay in pure mountain air, at a not too high altitude 
and where the barometer is not too low, is usually beneficial 
to neurasthenics. Daily systematic, but not forced, tramps in 
the mountains, continued for weeks, do more good sometimes 
than all the medicines of the pharmacopoeia taken during the 
long winter. The internal medicines are anyhow of not much 
avail in the treatment of neurasthenia. Iron, quinine, arsenic, 
the stomachics, all will disappoint us ; all will sometimes ac- 
complish nothing ; they rather tend to derange the digestion, 
and with this take away the last remnant of the patient's 
courage. The only drugs necessary will be such as are re- 
quired for the proper regulation of the bowels. 

Among the above-described symptoms there are two the 
treatment of which deserve special mention — first, the sleep- 
lessness ; secondly, the impotence. About the former nothing 
needs to be added to what has been said on page 162. To 
meet the latter much is to be expected — if, of course, organic 
disease, spermatorrhoea, and the like, have been excluded — from 
the local application of electricity. A large electrode, the 
anode, is placed over the lumbar cord, while the cathode is 
moved from the external inguinal ring down along the sper- 
matic cord or applied without being shifted (Erb). With this 
may be combined the application of the faradic brush over 
the whole genital region. One electrode, the cathode, may 
also be placed in the rectum, the other upon the sacrum or 
perineum (Mobius). Finally, a bladder electrode, which has 
the shape of a catheter, and which is insulated up to its metal- 
lic tip, may be introduced into the urethra as far as the fossa 
navicularis, while the anode is applied over the lumbar cord, 



NE URA S THENIA . 5 5 

and at the negative pole the current is made and broken sev- 
eral times. From this method, which has been recommended 
more especially for paralysis of the bladder and incontinence 
of urine, we have repeatedly seen good effects in the treatment 
of impotence. 

The feeding system of Weir Mitchell, which has also been 
recommended in neurasthenia, we shall discuss in the chapter 
on hysteria. 

LITERATURE. 

Beard. On Neurasthenia. New York, 1880. 

Eisenlohr. Deutsche med. Wochenschr., 1884, x, 21. (Differential diagnosis 
between tabes and neurasthenia.) 

Beard und Rockwell. Die sexuelle Neurasthenie. Wien, 1885. 

Mobius. Die Nervositat. Leipzig, 1885, 2. Aufl. 

Thayer. Neurasthenia. Phila. Med. and Surg. Report., 1886, liv, 17, 18. 

Berdt Hovell. On some Conditions of Neurasthenia. London, 1886, Churchill. 

Averbeck. Die acute Neurasthenie. Deutsche med. Ztg., 1886, vii, 30, 31. 

Langstein, H. Die Neurasthenie. Wien, 1886. 

Mitchell, S. Weir. An Essay on the Treatment of Certain Forms of Neuras- 
thenia and Hysteria. Phila.: Lippincott, 1885. 

Uherek. Die functionellen Neurosen beim weiblichen Geschlecht und ihre 
Beziehungen zu den Sexualleiden. Berlin: Neuwied, 1886. 

Clark. Some Observations concerning what is called Neurasthenia. Lancet, 
January 1, 1886, i. 

Krafft-Ebing, v. Ueber Neurasthenia sexualis beim Mann. Wiener med. 
Presse, 1887, xxviii, 5, 6. 

v. Ziemssen. Die Neurasthenie und ihre Behandlung. Leipzig: Vogel, 1887. 

Hanc. Ein seltener Fall sexueller Neurasthenie. Wiener med. Klinik, x, 5. 

Pippinskold. On neurastheniens forekomst bland kroppsarbetare. Finska 
lakaresallsk. handl., 1887, xxix, 11. 

Burkart. Berl. klin. Wochenschr., 1887, xxiv, 45. (Recommends Weir Mitch- 
ell's treatment.) 

Lowenfeld. Die moderne Behandlung der Nervenschwache. (Neurasthenia, 
hysteria, and kindred diseases.) Wiesbaden, 1887. 

Mathieu. Neurasthenie et hysterie combinees. Progr. med., 1888, xvi, 30. 

Lemoine. Pathogenie et traitement de la neurasthenie. Ann. med. psych., Sep- 
tember, 1888, 7me ser., viii. 

Webber. A Study of Arterial Tension in Neurasthenia. Boston Medical and 
Surg. Journ., May, 1888, cxviii, 18. 

Fiirbringer. Zur Kenntniss der Impotentia generandi. Deutsche med. Woch- 
enschr., 1888, xxv, 28. 

Wagner. Zur Begriffsbestimmung und Therapie der Neurasthenie. Schweizer 
Correspondenzbl., 1888, xviii, 9. 

Pelizaeus. Zur Differentialdiagnose der Neurasthenie. Deutsche med. Zeitg., 
1889, 27, 28. 



CHAPTER II. 

HYSTERIA. 

Hysteria has this in common with neurasthenia, that it 
does not depend upon any demonstrable anatomical lesions of 
the nervous system, but it differs from it in the fact that for 
its development a certain predisposition on the part of the pa- 
tient is absolutely necessary. Although we are not as yet in a 
position to say of what nature this predisposition is, we must 
assume that the whole nervous system of a hysterical patient, 
central as well as peripheral, is in some points, which we are 
still unable to determine, different from that of healthy indi- 
viduals. The increased impressionability, the hyperesthesia 
of the central nervous organs, the increased sensitiveness of the 
peripheral nervous system, the diminished energy with which 
influences coming from outside as well as from within are met, 
the lowered general power of resistance and self-control, these 
are on the whole the traits which characterize hysterical per- 
sons, and explain why the symptoms are so manifold and change 
so rapidly, and why in no other disease of the nervous system 
can be found a train of manifestations so diverse and so nu- 
merous. 

Only by unwearied, long-continued study has it been possi- 
ble to show that even for the apparently arbitrary appearance 
of the different symptoms there exist certain laws. In a man- 
ner which none before or after have been able to rival, hysteria 
has been studied by Charcot and his pupils, to whom we owe 
the most interesting observations and investigations of the past 
two decades. 

Symptoms. — For the sake of simplicity, we shall divide 
in our description of the disease the symptoms into cerebral, 
spinal, and mixed, that is, pertaining to the entire nervous 
system. 

The cerebral may again be subdivided into psychical and 



HYSTERIA. 507 

somatic symptoms. The disposition of the patients is excitable, 
anxious, often changeable, sometimes passing from the depths 
of gloominess to the most exalted hilarity. The tendency to 
speak of nothing else than of their own woes, the constant at- 
tempt to greatly exaggerate these, and to excite sympathy in 
their friends and physicians, the thoughtless demands which 
they expect to be satisfied at a moment's notice, and the incon- 
siderate outbreaks of anger if this is not done — all these are 
characteristic features of the disease with which we meet, not 
in all indeed, but at any rate in a large majority of cases. The 
tendency to get easily frightened is very common, and during 
a state of the highest psychical excitement hallucinations may 
temporarily exist. In pure cases of hysteria, however, we 
need never be afraid that these will persist long or lead to any 
serious outbreak on the part of the patient. Exceptionally an 
instance of " hysterical sleep " comes under our notice, into 
which the patient has fallen after certain prodromal symptoms 
have existed for several hours. The peculiarities of this curi- 
ous condition, the " lethargie hysterique," which may last for 
many days, the conditition of the organs of circulation and di- 
gestion, the characteristic signs by which the hysterical sleep 
may be discriminated from other states of coma, have recently 
been described by Gilles de la Tourette in a careful monograph 
(Arch, de neurol., 1888, 43, 44), to which the reader is referred 
for further information. 

Among the cranial nerves there is not a single one which 
may not at one time or another in the course of hysteria pre- 
sent symptoms of paralysis or irritation. More than the 
others the nerves of special sense are interesting for their 
anaesthesias and hyperesthesias. The nerves of smell and 
hearing are those most frequently affected, and both functions 
may be so much impaired that the patient can smell and hear 
nothing. They may, on the other hand, become so acute that, 
if we may believe her own statements, she is able to distin- 
guish any one from a number of perfumes, or to single out an 
individual by the sound of his voice amid the hubbub of a 
crowd, or again to recognize people far off by their step, and 
so forth. These and similar faculties have in Mesmer's time 
already been spoken of a great deal, and have given rise to 
much deception and trickery. The opticus is also not rarely 
affected. Besides the cases where hysterical patients suddenly 
become blind in one or both eyes without there being any 



5o8 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



changes in the disk, there are instances of decrease in the 
acuteness of vision, contraction of the field of vision, or com- 
plete or partial loss of color sense. When the last-named con- 
dition occurs the perception of blue and yellow is retained 
longest, while that of violet and green disappears much ear- 
lier. The ocular muscles rarely participate in the disease ; 
hysterical paralysis of them is exceptional, as is also the occur- 
rence of hysterical nystagmus, on which subject I have ex- 
pressed my opinion elsewhere (cf. lit.). 

Among the other nerves of special sense that of taste may 
occasionally present alterations. The patients lose their taste 
either completely or only for certain substances (sour, salty), 
or there may exist such a perversion of this faculty that every- 
thing tastes nauseous and disgusting, or that everything tastes 
of salt or of vinegar, and so forth. Actual hallucinations of the 
sense of taste, although not so frequent as hallucinations of the 
sense of smell, are not unheard of. 

The trigeminus is generally implicated. Faceache and 
headache, among others the kind which is confined to a small 
spot and is known as clavus, are comparatively frequent. The 
scalp is sometimes so markedly tender that the patients can 
not stand the slightest pressure, not even the touch of the 
comb, and in order to avoid the pain they abstain from all 
care and proper attention to the hair. The pain in the head 
may also be confined to one side, and resemble in every detail 
that of hemicrania. 

What needs to be said about the facial nerve in this connec- 
tion has already been treated of in Chapter V, Part II. Tic 
convulsif, as well as facial paralysis, may be hysterical in na- 
ture ; however, we must not forget that facial spasm and hys- 
teria may well coexist, and that a tic convulsif occurring in the 
course of hysteria is not necessarily of hysterical origin. The 
determination of this question is less important for the diag- 
nosis than for the prognosis. The outlook in non-hysterical 
tic is very bad, in the hysterical variety relatively favorable 
(Guinon, Revue de med., June, 1887). Of much interest are 
the many forms of vagus neuroses which we meet with in the 
course of hysteria; they may affect, in the manner described in 
Chapter VIII of Part II, the organs of respiration, circulation, 
and digestion. Among the first, not only the larynx, but the 
lungs also, are sometimes attacked. The laryngeal muscles 
become the seat of violent spasm, "hysterical spasm of the 



HYSTERIA. 50 9 

glottis," during which the patient is afraid she is choking. The 
functions of the vocal cords may become so much interfered 
with that the patient is only able to make herself understood 
in whispers — to speak out loud is impossible ("hysterical 
aphonia"). The laryngoscopical examination reveals nothing 
abnormal, with the exception of some anaesthesia of the mucous 
membrane of the fauces, which greatly facilitates the examina- 
tion (cf. page in). The respiratory muscles may be affected 
in a peculiar and very striking manner, the acceleration in the 
number of respirations may attain such a degree that, instead 
of fifteen or sixteen respirations a minute, we may count from 
eighty to one hundred. On the other hand, they may be dimin- 
ished in frequency, and the patient breathe from eight to ten 
times a minute, but in a labored way, showing signs of a regu- 
lar dyspnoea, not infrequently with audible wheezing in inspi- 
ration and expiration (" hysterical asthma "). A dry and bark- 
ing cough, which is distressing not only to the patient, but also 
to all who surround her, is sometimes observed, and paroxysms 
of yawning, sobbing, laughing, or crying (" hysterical laughing 
or crying fits"), may persist for hours. 

Sometimes following aphonia, sometimes occurring abrupt- 
ly, and unexpectedly without it, in rare instances a complete 
dumbness sets in ; the patient has either actually lost the con- 
trol of her speaking apparatus or will not make use of it ; in a 
word, she is completely mute, and no amount of admonitions, 
entreaties, or threats can succeed in eliciting a single word. 
This condition of " mutismus hystericus " may be of variable 
duration. In one instance which came under my notice the 
patient maintained silence from the fifth of September to the 
twenty-eighth of April of the following year. She found her 
voice again at once on hearing of the unexpected death of her 
mother (cf. the articles of Natier, Huysmann, and others). 

The circulatory organs, more especially the heart, take 
relatively the smallest share in the disease. Hysterical tachy- 
cardia may occur, but it is rare and never well marked ; 
even in the apparently severest attacks, which we shall de- 
scribe later, the pulse is quiet. To stenocardia we have re- 
ferred on page 121. 

The digestive tract and the muscles pertaining to it — which, 
just as the pharyngeal muscles, are innervated at least partly 
by the glosso-pharyngeal and not by the vagus alone — may be 
the seat of various hysterical manifestations. The muscles of 



cio DISEASES OF THE GENERAL NERVOUS SYSTEM. 

the pharynx may present symptoms of paralysis or of irritation. 
In the former case deglutition is much interfered with, and 
may, indeed, be impossible ("hysterical deglutition paral- 
ysis"). 

A peculiar affection of the muscles of the oesophagus, 
which are supplied by the vagus, consists in a spasmodic con- 
traction which gives rise to a very vivid sensation of a ball 
rising up from the region of the stomach and sticking in the 
throat. This " globus hystericus " is so frequently met with in 
hysteria and is usually so well marked that it has been looked 
upon as pathognomonic for the disease. 

The musculature of the stomach and the intestines is liable 
to disturbances. According to most authors, paralysis of these 
muscles produces a distention of the bowels and of the whole 
abdomen which may be simply enormous (•" meteorismus hys- 
tericus ") ; this is sometimes associated with colicky pains. A 
certain amount of the air, which frequently collects in large 
quantities in the bowels, escapes through the mouth with a 
loud, sobbing, gurgling noise (singultus, ructus hystericus). 
Talma (Weekblad van het Nederl. Tijdschr. voor Geneesk., 
1886, 9) claims that the cause of hysterical tympanites is to be 
sought in a spasm of the diaphragm. As evidence in favor of 
his view he argues that under chloroform narcosis the disten- 
tion will disappear without the emission of gas, and secondly, 
that the position of the diaphragm is abnormally low. 

Vomiting is one of the most frequent occurrences in hys- 
teria ; sometimes it is very profuse and may persist for hours, 
and be so intractable as to weaken the patient considerably ; 
on the other hand, slight vomiting may occur daily for weeks 
without affecting the patient's strength. Usually watery 
masses are thrown up which bear no proportion to the quan- 
tity ~ of food ingested. In one of my cases the amount vomited 
was eight or ten times as large as that taken in. 

Affections of the accessorius are not rarely seen in the form 
of spasmodic torticollis, while affections of the hypoglossus are 
very exceptional. 

One of the most remarkable cerebral affections which may 
occur in the course of hysteria is an apoplectiform attack with 
consequent hemiplegia, which in many instances is associated 
with complete hemianesthesia. This hemiplegia may develop 
with symptoms similar to those of the form following arterial 



HYSTERIA. 



5H 



disease, and, as we have already pointed out above, it may be 
extremely difficult to distinguish a hysterical hemiplegia from 
one due to organic disease. This is especially the case if there 
are no other hysterical symptoms to aid us. If the unilateral 
spasm of the muscles of the cheek described by Charcot, and 
before him by Brodie (1880), which is said to be characteristic 
of hysterical hemiplegia, be present, the diagnosis is easier. 
All the symptoms associated with a cerebral hemiplegia — for 
instance, tremor, the associated movements, even atrophy of 
the muscles of the diseased side — may accompany the hyster- 
ical variety. The opinion formerly prevalent, that wherever 
there exists atrophy this must needs depend upon an organic 
lesion in the brain, spinal cord, or the nerves, has been proved 
to be erroneous. The hysterical atrophy may not differ from 
that due to organic disease ; it may develop comparatively 
rapidly, may remain for a long time, and disappear again just 
as rapidly when motion returns. Fibrillary twitchings in the 
atrophic muscles and reaction of degeneration are absent. 
Whether the large ganglionic cells in the anterior horns have 
anything to do with the occurrence of atrophy, and, if so, 
what is the nature of the influence, we do not know (Babinski, 
Arch, de neurol., 1886, xii, 34, 35 ; cf. lit.). 

Among the spinal symptoms of hysteria motor and sensory 
paralyses play the most important role. With hysterical pa- 
tients we can not feel certain for a single day or hour that 
some sort of paralysis will not occur, for it is characteristic, 
we may say pathognomonic, of hysterical paralyses that they 
appear quite suddenly, and happily often disappear as quickly, 
it may even be after persisting for months and years. There 
is no characteristic distribution of the hysterical motor dis- 
turbances ; they may take in only one extremity, or may ex- 
tend to both legs or both arms, so that these are perfectly 
useless. Examination shows that the paralyses are usually of 
a flaccid type. We may frequently make the observation that 
the patients are not completely robbed of the use of the af- 
fected limbs, but that they have lost the will to use them. 
Especially is this apparent when they are asked to perform 
co-ordinated movements. A patient, though able to move the 
right arm, may assert that she is unable to write ; though she 
is able to move her legs, any attempt at walking is an utter 
failure; on rising, her legs give way' under her, and she simply 



512 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



is unable to keep herself on her feet. In short, the necessary- 
will power is gone. 

Symptoms of motor irritation — for instance, isolated mus- 
cular spasms — are far less frequent. Of much interest are the 
involuntary movements which are now and again observed. I 
had a lady under treatment who, without wishing it, but with- 
out being able to resist the inclination, would for hours at a 
stretch keep on raising both arms and letting them fall again 
without the least feeling of fatigue. 

Clonic muscular spasms, in the muscles of the face, as well 
as in the extremities, which, appearing in paroxysms, usually 
are symmetrical in their distribution, and are not sufficient 
to produce movements of the affected limbs, have been de- 
scribed by Friedreich as paramyoclonus multiplex, and by See- 
ligmuller as myoclonia congenita. That they are of hysterical 
origin is more than probable. The trouble is rare, and has 
probably always to be regarded as an emotional neurosis. The 
strength of the muscles and their electrical excitability remain 
unaltered, and sensory changes are absent. Sometimes there 
are tender points along the spine, which may be best treated 
by the anode of the constant current. Other measures are not 
necessary, especially as recovery seems to be the usual out- 
come (cf. lit.). 

Often combined with paralyses of the extremities are joint 
contractures, which as a rule appear suddenly, and may per- 
sist for months and years. When occurring in the upper 
extremities, in the elbow, in the wrist, and in the finger joints, 
they are usually flexor contractures ; in the knee and ankle 
joints, extensor contractures. The way in which they dis- 
appear under chloroform narcosis is very remarkable. In- 
dividual muscles may also be the seat of contractures, and 
we have described a case on page 384 in which during 
the erect posture a contracture in the quadratus lumborum 
made its appearance, which disappeared when the patient lay 
down. 

Among the sensory disorders the diminution or complete 
loss of sensibility is the most important ; this may be so exten- 
sive that the patients can feel nothing on any part of the sur- 
face of the body, not excluding the mucous membranes (con- 
junctivae, nose, tongue, mouth, vagina, rectum), so that we can 
touch them with the hot iron (thermo-cautery) or prick them 
with knives and needles, and they will not make the slightest 



HYSTERIA. 5 J3 

sign or attempt to draw away the part ; nay, more, there are 
cases in which the deeper tissues take part in the anaesthesia, 
so that folds of skin may be transfixed and fine needles thrust 
into the muscles down to the bone without the knowledge of 
the patient if she be blindfolded. Besides the general, we may 
meet with circumscribed spots of anaesthesia, anaesthetic zones, 
on the back, on the hands, etc. The hemianaesthesia, which is 
strictly confined to one side, and which implicates the mucous 
membranes as well as the skin, has already been mentioned. 
These sensory changes also may appear and disappear sud- 
denly. 

Less common are the hyperaesthesias, which probably never 
take in the whole body and never even one whole half of the 
body, but are usually confined to circumscribed areas, to cer- 
tain internal organs, or by preference to certain joints. These 
circumscribed areas, Charcot's hysterogenic zones, vary in 
their situation ; they may be on the back, on the chest, in the 
extremities, or elsewhere. Among the internal organs, in 
women the ovaries, in men and boys the testicles, are the 
parts that usually suffer. The ovarian hyperaesthesia, which 
Charcot has studied very carefully, is closely related to the 
" major attacks " to be described later. That it is actually the 
ovaries which give rise to the acute pain when pressure is 
made over them Charcot has proved on pregnant women ; 
during pregnancy the position of the ovaries is changed, and 
it was found that there was a corresponding change in the 
position of the tender points. The women who suffer from 
this hyperaesthesia are in Paris called " ovariennes." 

Neuralgiform pains, which often affect the joints and which 
are very obstinate, are so common in the course of hysteria 
that whenever we find a joint neuralgia we should think of 
and search for a hysterical basis. Brodie has subjected them 
to a very accurate study and has pointed out that it is at times 
extremely hard to differentiate between a neuralgia and an 
actual disease of the joint. The hip and knee are most usually 
attacked. The joint is painful, especially on pressure or on 
motion ; hence such patients are, as a rule, found in bed or 
lying on the sofa. On closer examination the pain proves not 
to be confined to one spot, but distributed over more or less 
large areas of the lower extremity. The patient cries out if 
pressure is made in the neighborhood of the hip or the knee 
or lower down over the malleoli. She seems to be especially 

33 



514 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

sensitive when watching and following our manipulations ; but 
if the physician is able to divert her attention, pressure over 
an otherwise painful point will often evoke no complaint. In 
the course of the disease the glutei may undergo some atrophic 
changes ; now and then transient swellings are noted. On the 
other hand, there are instances where hysterical joints are the 
only cause which keeps the patient persistently in bed, where, 
in spite of an inactivity lasting for years, not a trace of atrophy 
can be recognized, and where the general health shows no 
signs of impairment. All these and other spontaneous pains, 
which we need not dwell upon here, occurring in hysterical 
individuals are to be regarded as being of psychical origin, and 
therefore as pain hallucinations (Strumpell, Hoist). 

Among the abnormities of the secretory organs, those 
which concern the urine chiefly deserve our attention. Hys- 
terical patients may urinate very little and not without diffi- 
culty (ischuria). On the other hand, we find some who urinate 
frequently and pass almost incredible amounts (polyuria). In 
the former case the specific gravity is high and the solid con- 
stituents of the urine are increased in amount. In the latter 
the urine resembles almost clear water. It would be erroneous 
to assume that the small or large amount of urine always de- 
pends upon the amount of water ingested. Indeed, patients 
who drink hardly anything may void very large quantities of 
urine, while those who drink a good deal may pass only a few 
drops at a time. Here, again, as with the manifestations of 
hysteria in general, no hard and fast rule can be given, nor can 
anything certain or constant be said about the salivary and 
sweat secretions, since they are equally subject to variations. 

The combined hysterical manifestations — that is, those 
originating in the brain as well as the spinal cord — consist of 
the so-called " paroxysms " or " attacks," in which conscious- 
ness is not lost, as in epilepsy, but which are associated with 
convulsions. Vague pains, ructus, yawning, the globus hys- 
tericus, ischuria, etc., may constitute the premonitory signs, 
which are immediately followed by violent respiratory move- 
ments, regular respiratory spasms, with laughing, screaming, 
weeping, barking, and finally the climax is reached in muscular 
spasms and convulsions resembling those of epilepsy. During 
such paroxysms the whole body may be thrown from side to 



HYSTERIA. 



515 



side, and it may be impossible to restrain the patients, because 
they exhibit a strength far greater than that which they ordi- 
narily possess. After the fit, which may last from half an hour 
to an hour, has spent its force, there follows a condition of gen- 
eral prostration, which usually does not last long and is fre- 
quently accompanied by polyuria. It is just these attacks 
which make the " home treatment " for hysterical patients so 
very difficult or finally even impossible. It has been found bv 
experience that the sight of such patients — the sight of the 
various contortions into which their bodies are thrown and 
the grotesque positions they assume — has an injurious effect on 
the other members of the family, especially if there are young 
girls among them. Such a scene and the consequent mental 
excitement have been known to cause similar attacks in other 
girls. 

Duration and Course. — The duration and course of hyste- 
ria are by no means uniform, although this much may be said, 
that it is always chronic and may last for years and tens of 
years. There are patients who from the time of puberty until 
they have passed the prime of life and (if they are women) 
until after the menopause, are hysterical, and thus never attain 
to the full enjoyment of life. At the beginning of the trouble 
there is usually nothing more than a certain tendency to nerv- 
ousness, a certain proneness to eccentricities, annoying to the 
patient and still more so to the family. Soon, various pains, 
which are apt to frequently change their seat and to vary in 
intensity, make their appearance, and certain respiratory phe- 
nomena, perhaps shortness of breath or a barking cough for 
which physical examination reveals no cause, begin to attract 
our attention. 

Severe motor disturbances are by no means noted in all 
cases ; even contractures are not very common. On the other 
hand, there are few cases in which the sensibility does not at 
various times undergo striking changes. Anaesthesias and anal- 
gesias alternating with hyperesthesias, and neuralgias, especial- 
ly of the joints, and persistent headaches, all help to sour the 
disposition of the patient. During menstruation the condition 
is usually aggravated. The patient is still more excitable than 
usual, and her complaints are louder. In those, in whom the 
paroxysms are an important feature of the case, this is more 
especially true, and sometimes the first menstrual period is the 



5 i6 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



signal for the first attack, which is at regular intervals followed 
by -others. In many cases of hysteria, "attacks" never occur. 
The patients, indeed, may without any provocation have fits of 
crying, laughing and screaming, but no convulsions. In old 
age, at a time when the patients begin to become sexless, the 
hysterical phenomena fade. As the hair turns gray the dispo- 
sition becomes calmer and more equable, and even egotistical, 
exacting, peevish women, who have tormented their families 
continually and who were extremely hard to manage, become 
yielding, amiable old ladies after the hysterical manifestations 
have once left them. Still there are, unfortunately, exceptions 
where these persist even after the seventieth birthday. 

The prognosis may be inferred from our description of the 
course of the disease. Doubtful as it always is, it is made still 
more gloomy from the fact that persons who have for years 
suffered from hysteria are apt to be subject later in life to 
actual organic diseases, especially of the brain (Feldmann, In- 
augural Dissert., Leipzig, 1887). 

Hysteria was thought, as the name indicates, to occur ex- 
clusively in members of the female sex. That it is more preva- 
lent among them there can be no question, but Charcot and 
his pupils have shown convincingly that it does occur in men 
and boys, and that, too, much more frequently than might a 
priori have been supposed. From him we have learned that it 
occurs frequently among the French soldiers. Further inves- 
tigations may prove that this would hold good not only for 
the French, but also for other armies. Age seems to have 
much less influence than was at first assigned to it. Hysteria 
in children is by no means rare. The full development of all 
hysterical manifestations in the young, who are far from being 
sexually mature, proves that puberty and the sexual organs are 
of less importance in the causation of this neurosis than has 
formerly been supposed. 

Diagnosis.— The diagnosis of hysteria may at one time be 
very easy, at another we may encounter no inconsiderable diffi- 
culties. When we have an arraj- of ever-varying symptoms 
occurring apparently without order, when the patients com- 
plain to-day of this, to-morrow of that, while the physical signs 
show no grounds for their troubles, it does not need an expert 
to suspect and diagnosticate a hysterical condition. If, on the 
other hand, the disease sets in suddenly without previous dis- 



HYSTERIA. 



517 



orders of any kind, in one case with a hemiplegia, in another 
case with a severe hip trouble, it may be by no means easy to 
say whether and, if so, why the hemiplegia is of hysterical 
origin, and whether or not the joint affection is to be regarded 
as a hysterical coxalgia. 

The following points will in the majority of cases be found 
sufficient to clear up any difficulties which the diagnosis pre- 
sents : 

With regard to the cerebral symptoms, and more especially 
those belonging to the affections of certain of the cranial nerves, 
we have in previous chapters pointed out some features char- 
acteristic of the hysterical varieties. It will be necessary in 
every separate case to exclude scrupulously anatomical lesions 
and to determine whether there are in addition to those be- 
longing to the cranial nerves other symptoms which point to a 
hysterical condition. If such be found, and more especially if 
our objective examination gives negative results, the diagnosis 
of hysteria is warrantable. 

These rules are particularly applicable where we have to 
decide whether a hemiplegia is hysterical or due to a lesion in 
the internal capsule, whether a contracture has to be regarded 
as hysterical or cortical (page 184), and whether the disturb- 
ances of the respiratory organs depend upon diseases of the 
lungs or the larynx or are to be referred to a neurosis of the 
vagus or of the recurrent laryngeal nerve. 

The recognition of the hysterical nature of spinal manifesta- 
tions belonging to the motor apparatus may give rise to the 
greatest difficulties. It is upon the electrical examination that 
we must rely in deciding whether the paralysis of an extremity 
depends or not upon a peripheral cause — that is, upon a neuri- 
tis. A well-marked reaction of degeneration always points to 
a chronic inflammatory condition. The age of the patient is 
of some value. Hysterical paralyses occur between the ages of 
fifteen and thirty, and more particularly in women. Further, 
we observe almost always associated with hysterical paralyses 
grave sensory disturbances which are not necessarily present 
in the other kinds (cf. Lumbroso, Lo Sperimentale, Firenze, 
1887; reference, Neurol. Centralb., 1888, 7). The existence of 
muscular atrophy is not sufficient to determine the organic na- 
ture of the paralysis because an atrophy of muscles does not ex- 
clude hysteria, as we have pointed out on pages 234 and 5 1 1 (Bris- 
saud, Arch, de physiol. norm, et pathol., April, 1887, page 339). 



5" 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



Contractures, if of hysterical origin, set in suddenly, and are 
almost always accompanied by other hysterical manifestations, 
meteorism, ovarian hyperaesthesia, and ischuria. Where such 
symptoms are absent we must be very careful in our examina- 
tion and take into account the possibility of an anatomical 
lesion either of central or of peripheral origin (cf. Blocq, Des 
contractures, These de Paris, 1888 ; Progr. med., 1888, xx, page 

397)- 

Hysterical muscular spasms may be taken to be tetany, as 
the case of Caiger, in the Lancet of August 20, 1887, shows. 
To the frequent occurrence of rhythmical spasm in certain 
groups of muscles in hysteria, Pitres has drawn attention in an 
article in the Gaz. med. de Paris, 1888, 13. 

Trembling and shaking movements, which somewhat re- 
semble those of intention tremor as they become more marked 
on voluntary motion, have been noted, but are rare. The pos- 
sibility of mistaking such conditions for multiple sclerosis (or 
vice versa) should, however, always be kept in mind. In our 
account of the latter disease we shall come back again to the 
points for the differential diagnosis between the two conditions. 

The sensory changes in hysteria, the anaesthesias, affect, as 
we said, not only the skin, but also the deeper tissues, so that 
needles may be inserted down to the bone without being felt. 
Usually all qualities of sensation take part in the disorder, so 
that the so-called muscular sense is also lost and the patients 
are unable after closing their eyes to give any account of the 
position of their limbs. Pronounced anaesthesia is found dur- 
ing the hysterical paroxysms. An anaesthesia extending over 
the whole body and taking in all the mucous membranes is al- 
most always hysterical in nature. 

Hyperaesthesias and neuralgias occurring in hysteria are 
typical in that they are very changeable, so that to-day cranial, 
to-morrow spinal nerves are the seat of the pain. Neuralgias 
of joints, if organic disease can be ruled out and if they are 
very obstinate and resist all the ordinary therapeutic measures, 
may be safely looked upon as hysterical. The " attacks " may 
be mistaken for epileptic fits. The important point to remem- 
ber in this connection is that in the hysterical attacks con- 
sciousness is never lost as completely as in epilepsy. Biting of 
the tongue is an exception in the former. The hysterical at- 
tacks are, moreover, attended with noisy laughing and crying, 
etc., while epileptics, with the exception of the initial cry 



HYSTERIA. 



519 



(which is not constant), pass through the whole convulsive 
stage quietly and without uttering a sound. It has been 
claimed that there never occurs an elevation of temperature 
during the hysterical seizure, while the epileptic fit is accom- 
panied by a slight rise, 1.2 to i.8° F. This statement can not 
easily be controlled, and certainly needs further confirmation. 
Finally, it should be remembered that hysterical attacks may 
in some instances be produced by pressure upon the ovaries or 
the testicles, while in epilepsy this is never the case. 

Pathogenesis and ./Etiology. — About the nature of hysteria 
we are absolutely in the dark. Not one of the many attempts 
to explain the disease can be regarded as more than a vague 
hypothesis. This one fact may be regarded as certain, that 
the existence of grave anatomical changes is excluded or, at 
any rate, is highly improbable, otherwise the suddenness with 
which the symptoms come and go would be absolutely inex- 
plicable. The old idea that the uterus must be held responsi- 
ble in every case and under all circumstances for the disease, 
which was consequently called hysteria {vcrrepia), has been 
shown to be untenable by the number of cases observed in 
men and young children ; and the more cases we see, the clear- 
er it becomes that the hysterias occurring in males and in little 
children furnish a considerable proportion of the total number, 
and the more ridiculous becomes the term " hysteria," which 
sooner or later will be given up completely. The influence of 
the sexual organs on the disease will be discussed later, but we 
would state emphatically that the opinion that these are always 
the starting point of the disease is indefensible. 

But how shall we explain the disease ? If we agree that all 
symptoms of hysteria have certain characteristics in common, 
they may perhaps all together be traced to an increased excita- 
bility of the whole nervous system, to the quicker response 
to stimuli from without and within. Just as we have morbid 
conditions in which the excitability of the nerves and the mus- 
cles to the electrical current is found to be increased, we may 
imagine also an analogous condition in which all the nerves, 
including the nerve elements of the central organs of the brain, 
especially of its cortex, those of the spinal cord, and also of 
the peripheral nerves, are in a constant state of abnormal or 
pathological excitability. That in such a state the imagination 
plays an important role is self-evident — not, however, in the 



520 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

sense that all the sufferings of which the patient complains are 
imaginary and merely depend upon the imagination ; we rather 
mean that, in the condition described, mental conceptions are 
formed and disappear more quickly and are constantly chang- 
ing. Such a quick and unnatural change can not but exert an 
unfavorable influence, first upon the mind and disposition, and 
later upon the bodily condition. 

In reality it is in the majority of cases a disturbance of the 
psychical equilibrium which produces the disease. It is not 
impossible that careful study of the aetiology may do much 
toward a clearer understanding of the nature of the malady ; 
hence it seems in place to say a few words about the causes, as 
far as our limited knowledge will allow. They may be subdi- 
vided into direct and indirect. To the former belong a hered- 
itary, physical as well as psychical, predisposition of the indi- 
vidual. There is no doubt that only those persons can become 
hysterical who are a priori — that is, from birth — so predisposed, 
because they have a nervous system which presents the pecul- 
iarities which we have just described. This congenital, be- 
cause hereditary, predisposition finds favorable conditions for 
further development in (a) sex, {b) age, (c) education, (d) nation- 
ality or race of the patient. That the female sex and those 
just arriving at the age of puberty are prone to the disease we 
have said before, although the male sex and other periods of 
life besides that of puberty are by no means exempt. The 
hysteria which occurs in early childhood, and which has been 
observed between five and ten years of age, deserves special 
study (lit., page 530). 

Much must be attributed in the causation of hysteria to a 
faulty education. The brain may be overtasked at the ex- 
pense of the body, and, in consequence of too little firmness 
on the part of the parents, capriciousness, inconsiderateness, 
lack of truthfulness, of energy, and of will power, are fostered 
in the child, and, finally, when the children have behaved badly, 
the mysterious threats, especially of injudicious servants, of 
sending after them wild beasts, ghosts, " the black man," etc., 
can drive them into such a chronic state of fear that they can 
not go into a dark room without palpitation and the most in- 
tense feeling of terror. All such and many other mistakes in 
the early education of the child become indirectly causes of 
hysteria. As to race, the Slavonic (Poles, Russians), the Latin 
races (Frenchmen, Italians), and, above all, the Semitic, are 



HYSTERIA. e 2I 

more liable to hysteria than the Teutonic. The severest forms 
of hysteria are seen in French women and in Polish Jewesses. 
This may depend upon the national characteristics ; the lively, 
impetuous temperament which we find on an average more 
frequently in the Slavs, etc., than in the Germans, forms a par- 
ticularly favorable soil for the development of hysteria. 

Among the direct causes, disorders of the sexual organs 
play the most important part, and in both sexes this factor is 
equally potent. We must not think that the affection, which, 
especially in women, may, from a gynaecological standpoint, be 
very insignificant — for instance, a flexion or a change in posi- 
tion of the uterus — has in itself much to do with the matter ; it 
is much rather the idea that the trouble exists, and the anxiety 
lest it should interfere more or less materially with coitus and 
parturition, which constitute the direct cause of the depres- 
sion of spirits. The conjugal obligations — coitus, pregnancy, 
parturition — play such an important role in the life of every 
woman, if she has not missed her calling, that the mere idea 
that the sexual organs are diseased or incapable of performing 
their function is sufficient to give a severe shock to her hap- 
piness. In a man it is much less the potentia generandi than 
the potentia coeundi that causes him anxiety. The above-men- 
tioned psychical impotence, if it exist for a long time, in itself 
suffices to bring about a hysterical condition, and sexual neu- 
rasthenia is not rarely accompanied by pronounced hysterical 
manifestations, so that we can well speak of a coexistence of 
the two diseases. 

Secondly, traumatism ought to be mentioned as a possible 
cause of hysteria, and not only injuries which affect the body, 
but also those which concern the mind and the feelings — psy- 
chical traumatism. Above all, injury to certain parts of the 
body is interesting, inasmuch as such parts frequently become 
the seat of a hysterical affection ; thus we may after a lesion of 
the hip joint, after the injury has long been recovered from, 
find a hysterical coxalgia, and so forth. The psychical trau- 
matism may be of such a nature as to have an immediate 
influence, or may act gradually and insidiously. Among the 
former we have fright, emotions of anger, rarely of joy ; to 
the latter belong grief, anxiety, wounded self-respect or vanity, 
etc. Finally, there are traumatisms which, besides the bodily 
injury, also produce a mental shock ; among these may be 
mentioned injuries by lightning and the effect of accidents 



522 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



(fire, railroad accidents, etc.). The resulting " traumatic neu- 
roses," which in the case of railroad accidents have also been 
called railway spine, have in recent times been studied by 
Strlimpell and Oppenheim ; they are, without question, hys- 
terical in origin, although they present certain features which 
do not belong to the clinical picture usual in hysteria. Cases 
in which, in addition to the purely functional disturbances, 
definite anatomical changes in the nervous system are devel- 
oped in consequence of the accident, as, for instance, atrophy of 
the optic nerve, constitute the intermediate forms between the 
functional and the organic diseases. Of one thing we may be 
assured, viz., that a psychical will be more potent in its conse- 
quences than a physical traumatism ; the morbidly altered 
mind, by its abnormal reaction to the bodily ailments, consti- 
tutes and causes the lasting disease (Oppenheim) ; through a 
sort of auto-suggestion the sensory and motor paralyses de- 
velop in a similar way as the paralyses, and the like, which 
Charcot produced in hystero-epileptics by means of sugges- 
tion. 

The symptoms that appear after a person has been struck 
by lightning sometimes resemble the array of symptoms ob- 
served in traumatic neuroses. Paralyses in the nerves of spe- 
cial sense, and motor and sensory paralyses, appear and last for 
a shorter or longer time. In the spring of 1889, when thun- 
derstorms were so frequent, I had the opportunity of examin- 
ing a man who, as a consequence of being struck by lightning, 
on recovering consciousness after three quarters of an hour, 
presented loss of the power of sight and smell on the side 
where the lightning had entered and left the body, while on 
the same side hearing was diminished, and there was total an- 
aesthesia. These symptoms were associated with an obstinate 
insomnia. By hypnotism, frequently repeated, we were enabled 
to lessen this insomnia, and under the use of the galvanic cur- 
rent and the faradic brush the hemianassthesia disappeared. 
The nerves of special sense implicated became fully normal 
after a month's treatment. In this case motor disturbances 
were never seen. For further symptoms in such cases and for 
the post-mortem conditions found after death by lightning, we 
would refer the reader to Schmitz's article in the Deutsche 
med. Zeitg., 1887, 73, 74, where further references on the sub- 
ject may be found. 

The symptoms of " railway spine " are, as we might con- 



TRAUMATIC NEUROSES. 



523 



jecture from what has been said already, as manifold and as 
changeable as those of hysteria. Motor disturbances, manifest- 
ing themselves usually in a general motor weakness, are asso- 
ciated with abnormities of sensation, pains, especially in the 
head, paresthesias, hyperesthesias and anesthesias of different 
parts of the body, not excluding the nerves of special sense ; 
contraction of the field of vision, a certain decrease in the 
acuteness of sight, photophobia, disorders of the color sense, 
hyperesthesias of the nerves of hearing, smell, and taste, have 
been observed. Cutaneous anesthesias, mostly on the back 
over irregular areas, and even pronounced hemianesthesia hys- 
terica, anesthesias extending over the head, neck, and upper 
part of the chest (the so-called " doll's head " form), are often 
demonstrable, changes which vary with regard to their seat 
and extent in the same individual, so much so that frequently 
repeated examinations may give different results. The skin 
and tendon reflexes (as is the case in hysteria) are variable ; in 
the same way micturition is sometimes normal, sometimes dis- 
turbed. In walking, and in general in all movements of the 
body, the patient avoids as much as possible all motion of the 
vertebral column. He fixes the trunk and moves forward hold- 
ing his back stiff, and in every change of position makes as 
much use as possible of his hands (Oppenheim). Psychical 
anomalies, although they may be entirely absent, are usually 
present; they may manifest themselves by feelings of anxiety, 
depression, abnormal irritability, and hypochondriacal notions, 
which may eventually go so far as to lead to suicide ; some- 
times we encounter the so-called phobias, of which agorophobia 
is one of the most common. 

In every traumatic neurosis we must take into account the 
possibility, if not of complete simulation, at least of a tendency 
to exaggeration on the part of a patient; this is a difficult ques- 
tion to deal with, and great caution is necessary in view of a 
possible deception, but it would be quite wrong to go to the 
other extreme and regard all the patient's complaints and woes 
as belonging to the realm of fiction, and designate them as 
falsehoods. The legal bearing of such accident cases makes 
it here more especially the absolute duty of every physician 
to make a careful and unprejudiced examination, and it is not 
sufficient to look the patient over once, but a repeated study 
of him is necessary before giving a certificate. 

Finally, we would add that under certain circumstances the 



524 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



occupation of the patient may lead to hysteria. Working in 
certain poisons, especially quicksilver and carbon bisulphide, is 
said to be especially dangerous. Indeed, French writers speak 
of a definite mercurial and of a carbon-bisulphide hysteria. 
We shall return to this subject later. 

Treatment. — The treatment of hysteria is always a very 
tedious matter, and for the physician sometimes the most tire- 
some and thankless task imaginable and one to which he should 
only devote himself if he be assured of the implicit confidence 
of his patient, as far as this is possible in the case of hysterical 
individuals. This confidence is indispensable, because the treat- 
ment of the disease does not consist in the main in the admin- 
istration of drugs in a routine fashion, valerian, asafcetida, cas- 
toreum, and the nervines, but must depend more upon the 
psychical influence by which we endeavor to diminish the ab- 
normal sensitiveness of the patient to external and internal 
stimuli, to arouse her energy and to strengthen her will pow- 
er. This is, we admit, much more easily said than done, and 
we shall often have to confess that the patient's views about 
her trouble have not changed in the least, that she is as irri- 
table as ever, that her moodiness and capriciousness are in no 
way improved in spite of all our lectures — in a word, that we 
have obtained no positive result after " preaching reason " for 
hours. Still, we must not allow ourselves to become discour- 
aged, but ever again and again renew our efforts to obtain the 
desired end. 

If we clearly see that these are fruitless, and especially if 
we are convinced, as is often the case, that the family, far from 
assisting the physician, are virtually acting against him during 
his absence, we must impress upon them the necessity of re- 
moving the patient to some institution. French physicians lay 
the greatest stress upon isolation in such cases and are inclined 
to attribute the relatively favorable results of their treatment 
to this factor. In this country people are not so easily per- 
suaded to agree to this procedure as in Paris, where in the city 
itself or in the suburbs there are various admirably conducted 
institutions which only receive hysterical patients. With us, 
therefore, home treatment ought first to be tried. In France 
this is usually discarded from the first. It is a different matter, 
of course, if we have not to deal with a mild degree of hys- 
teria, but with hystero-epilepsy and major attacks. Then a 



HYSTERIA. 



525 



transference to an institution, as soon as practicable, ought to 
be urged. 

The bodily treatment may either be general (that is, di- 
rected to the nutrition, to the condition of the blood, and the 
strength of the patient) or symptomatic (that is, intended to re- 
lieve the troubles of the patient as they arise). 

With reference to the nutrition, it was Weir Mitchell and 
Playfair who first recommended absolute rest in bed, with mas- 
sage, electricity, and copious feeding. Their patients were 
forced to take considerable quantities of milk, meat, bread, etc., 
and it was found that with the increase of the body weight the 
hysterical symptoms and attacks diminished. Of late years 
good results have been obtained from this practice by Bins- 
wanger (Allgem. Zeitschr. f. Psych., 1883, xl, 4), and the com- 
munications of Leyden (Berl. klin. Wochenschr., 1886, xxiii, 16) 
and Burkart (ibid., 1886, 16) should encourage us to further 
trials with this method, although as far as my own experience 
goes the results have by no means always been brilliant. The 
cases in which the excessive ingestion of food was badly borne 
and led to a disagreeable gastric catarrh were by no means un- 
common, and even where the food was well assimilated the de- 
sired results were not always obtained. That much attention 
has to be paid to the nutrition there can be no question, and 
the increase in the body weight usually can be regarded as a 
favorable indication. To attain this, however, in many cases, 
not absolute rest, but, on the contrary, systematic muscular ex- 
ercise is needed. Well-regulated home gymnastics, under- 
taken according to definite principles (Schreber, Angerstein, 
and Eckler), are to be preferred and will be often found an ex- 
cellent means of combating the distressing insomnia. 

In certain cases, to be selected, of course, with care, general 
faradization as recommended by Beard and Rockwell is of 
great service. The patient for this purpose is placed upon a 
stool with his bare feet upon a moist large electrode, which is 
connected with the negative pole of the secondary coil. With 
the anode, which consists of a large sponge electrode, all parts 
of the body are treated in succession. Instead of the moist we 
may avail ourselves of a dry electrode in the form of a soft 
brush. The pain which is caused by the latter method is, at 
least with strong currents, quite considerable ; nevertheless, the 
method deserves warm recommendation in certain hysterical 
affections and especially in joint neuralgias. 



526 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

About the influence and the value of static electricity as a 
therapeutic agent our experience is not sufficient to warrant 
any definite conclusions. It is not easy to judge of the useful- 
ness of the treatment, as it is usually combined with other 
measures, the therapeutic significance of which must not be. 
left out of consideration. Whether the action of static elec- 
tricity differs essentially from that of the faradic and galvanic 
current, and, if so, in what this difference consists and under 
what circumstances the one or the other is indicated, we are 
not as yet in a position to say. The great inconvenience and 
expense of the apparatus militate greatly against its general 
introduction. 

It is rare that we treat a case of grave hysteria without at 
one time or another during the course of the disease being 
obliged to resort to massage ; for one thing, because the pa- 
tient desires as much variety as possible — but at the same time 
we must not overlook the fact that by its use many of the pa- 
tient's troubles are considerably relieved. This is not the place 
to enter into the minute details of this method of treatment. 
They may be found in the writings of Schreber, Reibmayr, 
Zabludowski, and others. 

The cold-water treatment is indicated where we desire to 
harden the constitution against external influences, changes of 
temperature, etc. We should be very careful, however, with 
low temperatures, and the water with which the patient is 
sponged or in which hip baths and the like are taken ought to 
be at least 8o° F. For the use of ice-cold douches, in the way 
recommended by the French, certain facilities are requisite. 
The pressure of the water should be very great and the dura- 
tion of the bath should be so short (from ten to fifteen seconds) 
that the patient has not time to become aware how cold the 
water really is. I have watched this practice repeatedly in 
some of the well-known hydrotherapeutic establishments of 
Paris and have had occasion to notice the immediate beneficial 
effects following the application. The lasting results, as Char- 
cot and others are quite convinced, are so marked that (in 
Paris) cold douches are considered to be indispensable in the 
treatment of hysteria. It would be a very desirable thing if 
the necessary arrangements for this treatment could be intro- 
duced into our hydrotherapeutic institutions. The ordinary 
shower bath, which comes down upon the patient just about 
like rain, is, of course, not sufficient. In the treatment of some 



HYSTERIA. 527 

of the particularly distressing symptoms it is, of course, in the 
first place the paroxysms which deserve our attention, because 
they, more than any other of the hysterical phenomena, are 
liable to render home treatment almost impossible. We may 
sometimes be able to cut short an attack by steady pressure 
with the hand over the ovaries continued for some time, but 
this can be better accomplished by allowing the patient to in- 
hale a little chloroform. To guard against a repetition of the 
attacks we have no reliable means, yet cool prolonged baths 
with affusions of colder water deserve a thorough trial. If 
these do not seem to be beneficial, and if the patient complains, 
before the onset of every attack, of pains in the ovarian region, 
and if we, moreover, can succeed in bringing about an attack 
by pressure over the (tender) ovaries, the question of oophorec- 
tomy has to be considered. The family relations, especially 
the sterility which naturally follows the operation, have to be 
taken into consideration, nor should we forget that the opera- 
tion has often by no means been followed by the desired effect, 
although the fact that it frequently exerts a favorable influence, 
as Hegar and Schroder have seen, can not be questioned. 
Whether the ovaries are actually diseased or not is altogether 
of minor importance. It is the presence of pain immediately 
before or after the attack in the region of these organs which 
should suggest an operative interference. Cauterization of the 
clitoris, advised by Friedreich, is a procedure which should 
only be resorted to in the most exceptional cases. In all in- 
stances the sexual organs ought to be carefully examined, and 
small operations, such as dilatation of the cervical canal, repo- 
sition of the uterus when in a position of flexion or version, if 
indicated, should be undertaken. Vaginismus, if it exists, should 
also be treated. 

The motor and sensory disturbances have to be met in 
the manner indicated above. In cases where we suspect ma- 
lingering or willful exaggeration, procedures which are disa- 
greeable or even painful are to be preferred — for instance, the 
cold baths, the faradic brush, the actual cautery, etc. The 
more minute details of the treatment must be left to the per- 
sonal tact of the physician, whose capability of individualiza- 
tion, of treating every case by and for itself, should make it 
unnecessary for us to enlarge upon all the principal phases of 
this disease. With regard to the internal medication, let it 
suffice to warn against the use of narcotics, especially morphine, 



528 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

which can not be given in a disease of such long duration in ef- 
fectual doses without creating the habit. 

LITERATURE. 

I. General. 

Hasse. Krankheiten des Nervensystems. In Virchow's Handbuch der spe- 
ciellen Pathologie und Therapie. Erlangen, 1869. (Contains the references 
to the older articles.) 

Briquet. Traite clinique et therapeutique de l'hysterie. Paris, 1859. (Basis 
of all French studies on hysteria.) 

Charcot. Lectures on Diseases of the Nervous System, delivered at the Sal- 
petriere. Translated by George Sigerson. New Sydenham Society, Lon- 
don, 1877. 

Charcot. Neue Untersuchungen iiber die Krankheiten des Nervensystems, be- 
sonders iiber Hysterie. Translated into German by Freud. Wien und 
Leipzig, 1886. 

Freud. Beitrage zur Casuistik der Hysterie. Wien. med. Wochenschr., 1886, 
49, 50. 

Mobius. Ueber den Begriff der Hysterie. Centralbl. f. Nervenheilk., 1888, 

xi, 3- 
Thermes. Traite elementaire d'hygiSne et de therapie de l'hysterie. Paris, 

1889. 
Charcot. Lecons du Mardi a la Salpetriere. Paris, 1889. (Policlinique, 1887— 

'88.) 

II. Special. 

a. Symptoms. 

Parinaud. Annal. d'oculiste, xcvi, 1886, 1 2. (Anaesthesia of the retina.) 

Bock. Hysterische Stummheit. Deutsche med. Ztg., 1886, vii, 103, 104. 

Cartaz. Du mutisme hysterique. Progr. med., 1886, 2me ser., iii, 7, 9. 

Brissaud et Marie. Progr. med., 1886, xv, 5, 7. (Deviation faciale dans 1'hemi- 
pl. hyst.) 

Charcot. Progr. med., 1886, xiv, 46. (Hysterical mutism in a man.) 

Guinon. Revue de med., 1887, vii, 6. (Tic convulsif.) 

Huet. Hysterische Facialisparese. Nederl. Weekbl., 1887, ii, 22. 

Borel. Ann. d'oculiste, 1887, xcviii, 5, 6. (Hysterical affection of the eye mus- 
cles, etc.) 

Schlesinger. Wien. med. Bl., 1888, xi, 3. (Stomach neurosis.) 

Natier. Contribution a l'etude du mutisme hysterique. Revue mens, de laryn- 
gol., etc., May, 1888, ix, 5. 

Huysman. Mutismus hystericus. Nederl. Tijdschr. voor Genesk-Fest. Don- 
ders' Jubelf., 1888, p. 394. 

Savill. Lancet, ii, August 7, 1888. (Hysterical aphonia in a woman seventy- 
one years old.) 

Peck. New York Medical Record, March, 1888, xxxiii. (Hysterical coma.) 

Robinson. Hysterical Dysphonia. Phila. Medical and Surgical Reporter, No- 
vember, 1888, lix. 

Babinski. Arch, de neurol., July, 1886, xii. (Atrophy in hysterical paralysis.) 



HYSTERIA. 



529 



Chauffard. Gaz. hebd., 2me ser., 1886, xxiii, 21. (Atrophy of the left upper 

extremity, hysterical monoplegia in consequence of traumatism in a young 

man.) 
Massalongo. L'atrofia muscolare nelle paralisi isteriche. Napoli: Detken, 1886. 
Debove. De l'apoplexie hysterique. Arch, gener. de med., 1886, No. 34. 
Voisin. Arch, de neurol., 1886, xii, p. 202. (Hysterical monoplegia of six 

months' standing cured instantly by suggestion.) 
Oserezkowski. Zur Diagnose der hyster. Hemiplegie. Centralbl. f. Nerven- 

heilk., 1887, x, 6. 
Martinencq. Cas d'apoplexie hyst. avec autopsie. Ann. med.-psych., March 7, 

1887. 
Brissaud. Arch, de phys. norm, et pathol., 1887, 3. (Hysterical hemiplegia 

with atrophy.) 
Achard. De l'apoplexie hysterique. Arch, gener. de med., January, 1887. 
Moravsik. Centralbl. f. Nervenheilk., 1888, xi, 20. (Hysterical symptoms in 

brain syphilis.) 
Sonques. Hemiplegie hysterique (chez un saturnin). Gaz. de Paris, 1889, 2. 



Kershaw. Lancet, 1887, ii 9. (Hysterical spasms resembling tetany.) 
Pitres. Gaz. de Paris, 1889, 17-26. (Rhythmical spasms.) 
Thijssen. Spasme glosso-labial hysterique. Nederl. Weekbl., 1888, i, 24. 
Foster. New York Medical Record, July, 1888, xxxiv. (Oesophageal spasms in 

a child.) 
Duret. Deformation de la region lombaire de nature neuro-musculaire (kypho- 

scoliose hysterique). Nouv. iconogr. de la Salpetr., 1888, 5. 
Audry. Du pseudo-mal de Pott hysterique. Lyon med., 1888, Ivi, p. 235. 
Hirt. Bresl. arztl. Zeitschr., 1888, x, 4. 

Paramyoclonus Multiplex. 
Friedreich. Virchow's Archiv, 1 881, Bd. 86, p. 421. 
Lowenfeld. Bayer arztl. Intell.-Blatt, 1883, xxix, 15. 
Marie, P. Progres med., 1886, xiv, 8, 12. 
Seeligmiiller. Deutsche med. Wochenschr., 1886, xii, 24. 
Francotte. Observations neuropathologiques. Liege, 1887. 
Homen. Finska lakaresallsk. Handl., 1887, xxix, 1. 
Bechterew. Arch. f. Psych, und Nervenkrankh., 1887, xix, 1. 
Vanlair. Des myoclonies rhythmiques. Revue de med., 1889, 1, 2. 
Kowalewski. Archivio italiano per le mal. nerv., 1887, xxiv, p. 288. 
Venturi. Giornale di Neurop., 1887, v, Fasc. 2. 
Starr, Allen. Param. Mult., with a Report of a Case. Journal of Nervous and 

Mental Diseases, 1887, xiv, p. 416. (Spasms appeared first after the patient 

had lifted heavy objects.) 
Rybalkin. Analyse. Petersb. med. Wochenschr., 1887, 44, p. 366. 
Marina. Ueber Param. mult, und idiopathische Muskelkrampfe. Arch. f. 

Psych, und Nervenkr., 1888, xix, 3, p. 684. 
Ziehen. Ueber Myoclonus und Myoclonic Ibid., 1888, xix, 2, p. 465. 
Zesas. Zur Differentialdiagnose der Gelenkneurosen. Chir. Centralbl., 1886, 

xiii, 16. 
34 



53Q 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



Pitres. De l'analgesie chez les hysteriques a 1'etat de veille et dans le sommeil 

hypnotique. Journ. de med. de Bordeaux, 1886, 50. 
Miiller. Mitth. d. Vereines d. Aerzte in Steiermark, 1886, xxii. (Interesting 

sensory disturbances.) 
Lichtwitz. Les anesthesies hysteriques des muqueuses et des organs des sens et 

les zones hysterogenes des muqueuses. Paris, 1887. 
Falcone. Deutsche med. Wochenschr., 1886, xii, 41. (Spontaneous falling out 

of the nails.) 
Ward. Phila. Medical and Surgical Rep., 1887, lvii, 5. (Hysterical spitting of 

blood.) 

b. ALtiology and Occurrence. 

Hysteria in Men and Children— Traumatic Hysteria — Railway Spine. 

Debove. Gaz. des hop., 1886, 20 (Hyst. chez l'homme.) 
Tuczek. Berl. klin. Wochenschr., 1886, xxiii, 31-33. 
Freud. Wiener med. Blatter, 1886, ix. (Hysteria in the male.) 
Dreschfeld. Med. Chronicle, 1886, v, 3. (Hysteria in the male after trauma- 
tism.) 
Duponchel. L'hysterie dans l'armee. Revue de med., June 6, 1886, vi, 
Janssen. Nederl. Weekbl., 1887, ii, 13. (Hysteria in soldiers.) 
Riesenfeld. Hysterie bei Kindern. Inaug. Diss. Kiel, 1887. 
Dubois. Schweizer Correspondenzbl., 1887, xvii, 13. (Hysteria in men and 

children.) , 

Coustan. Arch, de med. et de pharm. mil., 1887, x, 5. (Hysteria in the male.) 
Handford. British Medical Journal, October, 1887, 22. (Hysteria in the male.) 
Datil. Gaz. de Par., 1887, 53. (Influence of lead.) 
Guinon. Ibid., 1887, 48. (Influence of mercury.) 
Moricourt. Gaz. des hop., 1887, 6. (Hysteria in the male.) 
Engelsberg. Wiener med. Wochenschr., 1888, xxxviii, 14. (Patient a boy of 

thirteen years.) 
Lees, David. Lancet, June 23, 1888, i. (Hysteria in two boys.) 
Ray. Hysteria in the Negro. New York Medical Record, July 2, 1888, xxxiv. 
Clark. Journ. of Ment. Sc, January, 1888, xxxiii. (Hysteria in the male.) 
Guillemin. Ann. med.-psychol., March 7, 1888. (Influence of alcohol.) 



Charcot. Progr. med., 1885, xiii, 18. 

Oppenheim. Archiv f. Psych, und Nervenkrankh., 1885, xvi, 3. 

Troisier. Gaz. hebd., 1886, 2me ser., xxiii, 18. (Hysterical paralyses in conse- 
quence of traumatism.) 

Charcot. Wiener med. Wochenschr., 1886, xxxvi, 20, 21. (Hysterical coxalgia 
in the male as a consequence of traumatism.) 

The same. Progr. med., 1887, xv, 6. (Hystero-traumatic paralyses.) 

Debove et Catrin. Remarques sur l'hysterie traumatique. Gaz. hebd., 1887, 
2me s£r., xxiv, 43. 

Oppenheim. Berl. arztl. Correspondenzbl., 1887, 5. 

Vibert. Ann. d'hyg. publ., Dec, 1887, xviii, 12. (Railway spine considered 
from a medico-legal standpoint.) 

Lyon. Encephale, 1888, viii, 1. (Hysteria after severe injury.) 



HYSTERIA. 



531 



Charcot. Arthralgie hystero-traumatique du genou. Progr. med., 1888, xvi, 4. 

Bernhardt. Deutsche med. Wochenschr., 1888, 13. 

Striimpell. Ueber die traumatischen Neurosen. Berl. Klin. Fischer, 1888, 

3. Heft. 
Grasset. Hystero-traumatisme. Lecons recuedlies. Montpellier, 1888. 
Opfer, F. Beitrage zur Lehre von den traumat. Affectionen des Riickenmarks. 

Inaugural Dissertation. Berlin: Schade, 1888. 
Oppenheim. Deutsche med. Wochenschrift, 1888, x, p. 194. 
Baginsky. Berl. klin. Wochenschr., 1888, 3. 
Wolff. Ueber Railway-spine. Deutsche med. Ztg., 1888, 79, 80. 
Oppenheim. Die traumatischen Neurosen. Berlin, 1889. (With numerous 

references.) 
Bernhardt. Von den allgemeinen und traumatischen Neurosen. Berl. klin. 

Wochenschr., 1889, 18. 
Stepp. Deutsche med. Wochenschr., 1889, 4. 

Grasset. Lecons sur l'hystero-traumatisme. Paris: Lecrosnier, 1889. 
Meyer, Moriz. Berl. klin. Wochenschr., 1889, 5. 
Auerbach. Die traumatische Hysterie beim Manne. Inaugural Dissertation. 

Strassburg, 1889. 
Striimpell. Ueber traumatische Hysterie. Miinchner med. Wochenschrift, 

1889, 11. 

c. Treatment. 

Stein. Die allgemeine Elektrisation des menschlichen Korpers. Halle, 1883, 2. 
Aufl. 

Widmer. Schweizer Correspondenzbl., 1886, xvi, 9-1 1. (Cure by castration.) 

Reibmeyer. Die Technik der Massage. Wien, 1886, 2. Aufl. 

Tait, Lawson. Lancet, 1887, ii, 25. (Cure effected by the removal of pessaries.) 

Pitres. Progr. med., 1887, xv, 8. (Static electricity.) 

Greffier. De l'electricite statique et des ses applications a la therapeutique. 
Paris, 1887. 

Zubludowski. Zur Indication und Technik der Massage. Berl. klin. Wochen- 
schr., 1887, 36. 

Burkart. Berl. klin. Wochenschr., 1888, xxiv, 45-47. 

Gittermann. Deutsche med. Ztg., 1888, ix, 24. (Feeding system.) 

Didier. Sur l'electricite' faradique dans l'hysterie. Lyon med., 1888, lviii, p. 
356. 

Dutton. Lancet, June 23, 1888. (Massage, feeding system, seclusion.) 

Bielschowsky.. Ueber Influenzelektrizitat etc. Therap. Monatshefte, March, 
1880. 



CHAPTER III. 

EPILEPSY — FALLING SICKNESS — MORBUS SACER — MORBUS COMITIALIS. 

By epilepsy in the stricter sense of the term we designate a 
functional neurosis, the seat of which is still unknown, charac- 
terized chiefly by attacks of unconsciousness, with or without 
convulsions. In its wider sense the designation also comprises 
certain affections which are due to lesions of the brain and 
more especially of the brain cortex. For these it is less the 
loss of consciousness than the appearance of convulsions which 
is characteristic. To the latter kind of epilepsy belongs the 
so-called Jacksonian, partial, or cortical epilepsy (cf. page 184). 
A most conscientious examination and a correct answer to the 
question, whether the attacks constitute alone the disease or 
whether they are merely a symptom of a primary affection 
which is attended with still other manifestations, are for the 
patient as well as for the physician of the greatest importance, 
as this will be of importance for the treatment as well as for 
the prognosis. We shall first only give our attention to the 
so-called " genuine " or idiopathic epilepsy. 

The manner in which an epileptic patient can spend his life, 
the possibility of doing justice to the requirements of his call- 
ing and of being a more or less useful member of society, the 
outlook for improvement or even recovery — all these questions 
depend in the main upon the " attacks " to which he is subject, 
on their nature, their duration, their frequency, their after- 
effects, and so forth. Hence it is our first duty in taking 
charge of a case of epilepsy to study carefully the attack itself. 

Symptomatology. The "Attack." — There are cases in 
which the attack occurs suddenly and unexpectedly, so that 
the patient, until now in apparently perfect health, falls to the 
ground as if struck by lightning. In others — more numerous — 
it is announced, so to speak, by certain premonitions, which, to 
maintain Galen's old expression, we call auras. 



EPILEPSY. 533 

In the study even of the aura we can not help being struck 
with the fact which, on a closer examination of the attack, is 
still more impressed upon us, that no two cases of epilepsy are 
alike, that almost every one has its own peculiarities, so that a 
general description is almost impossible. The premonitions 
are countless and many attempts have been made to divide 
them into classes. Even if we have obtained a classification we 
are far from possessing with it a description of all. 

First of all, we may subdivide the auras into psychical and 
somatic. In the former case the patient may either become 
surprisingly quiet and look meditative, or he may present 
signs of excitement, walk anxiously up and down the room, 
and seem bewildered. The transition from the aura to the 
actual pre-epileptic disturbance of consciousness, the pre-epilep- 
tic insanity, is not appreciable (Mendel, Eulenberg's Viertel- 
jahrsschrift, N. F., 1885, Bd. 42, Heft 2). This prodromal 
state may extend over several hours, although it may not last 
any longer than thirty seconds or a few minutes. In two 
cases the patients told me that, immediately before the attack, 
reminiscences of bygone days forced themselves upon their 
minds, and that portions of their past lives rapidly passed 
before them. A psychical aura of this kind is rare. Some- 
times an irresistible desire in the patient to run constitutes 
the aura. Just as we shall see in the form of epilepsy called 
epilepsia procursiva, the patient escapes from his home and 
runs great distances. While he is running he is seized with 
the attack. Midway between the cases where there is a psy- 
chical and those where there is a somatic aura we shall place 
those instances in which the patients complain of vertigo, 
violent headache, and slight disturbances of consciousness, 
symptoms which also may last but a very short time, and 
which, indeed, may be of such brief duration that the patient 
has not time to guard himself against falling. Here, too, be- 
long the hallucinations which occur in the domain of the 
nerves of special sense, which we are accustomed to call 
" special sense " auras. The patient hears, sees, smells, tastes 
things which either are not there at all or are in reality differ- 
ent from what he deems them. I know instances in which im- 
mediately before the fit the patient thinks he is standing in a 
sea of light ; most intense brightness surrounds him, and he is 
cognizant of wonderful light effects. In other cases again the 
patient thinks he is standing amid utter darkness, he sees noth- 



534 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



ing, and the densest obscurity reigns everywhere. To this 
class belong the instances reported by Heinemann where bi- 
lateral amauroses constituted the aura (Virchow's Arch., 102, 
3, 1885, page 522). The optic as well as the auditory auras 
vary in different patients. Sometimes they hear delightful 
melodies, sometimes they find themselves amid the wildest tu- 
mult of confused noises. Complete loss of hearing, transient 
deafness, which would be analogous to the transient amauro- 
sis, I have never had an opportunity to note. 

Sometimes, not often, the patients imagine they hear dis- 
tinctly different voices. Then the aura is a genuine hallucina- 
tion and infringes upon the domain of pre-epileptic insanity. 
Well-pronounced gustatory and olfactory aurae do occur, but 
are decidedly less frequent than those just described. 

The somatic auras are either motor, sensory, or vaso-motor. 
The motor more frequently consist of symptoms of irritation 
than those of paralysis. There are isolated twitchings in the 
fingers or toes, in the arms or legs, which progress from the 
periphery to the centre ; contractures in some fingers have 
also been observed. In addition to or in the place of these 
there may be twitching movements of the head or neck, twitch- 
ings of the facial muscles, or well-marked strabismus. Paretic 
symptoms, heaviness and fatigue in the extremities, are more 
rare. Spasm of the glottis, bronchial asthma, palpitation of 
the heart, retching — all have to be regarded as varieties of 
motor auras. 

The sensory auras consist of peculiar parassthesias in the 
extremities, formication, numbness in the fingers, the patient 
feeling as if these were working their way up to the head or to 
the heart. Not uncommonly they are associated with a pro- 
nounced feeling of anxiety and oppression. The sensations 
which appear in the extremities, sometimes in the fingers, 
sometimes in the toes, are extremely variable, from a pleasant 
slight tingling to a painful burning and stinging, which, as we 
have said, proceeds from the periphery to the centre. 

In vaso-motor auras the hands become cold and pale, the 
cutaneous veins look less full than normally, and the patient 
complains that he is getting cold. A general feeling of chilli- 
ness, associated with chattering of the teeth, has also been 
noted (Douty, Lancet, March 20, 1886). In other instances, 
possibly on account of a paralysis of the vaso-motor nerves, 
blushing of the skin and sweating occur. The degree of full- 



EPILEPSY. 



535 



ness of the cutaneous vessels and the larger veins of the skin 
is in some cases sufficient to tell the patient whether or no the 
will shortly have a fit. 

Innumerable transition forms and countless combinations of 
different kinds of auras occur. No definite laws can be given, 
and we must here again recall the inexhaustible varieties of the 
prodromes by which the attack may be ushered in. 

The question whether the origin of the aura be central or 
peripheral can as yet not be answered. Certain facts point to 
the first possibility, others to the second (cf. Oliver, Lancet, 
April 21, 1888, page 769). That the aura may have an anatom- 
ical basis is proved by the case reported by Hughlings Jack- 
son (Brit. Med. Journal, February 23, 1888). The patient, a 
man of fifty-three years of age, complained regularly of a hor- 
rible, indescribable stench which immediately preceded every 
attack. At the autopsy a tumor was found situated in the 
temporo-sphenoidal region. We would remark, by the way, 
that this case is a point in favor of Ferrier's localization of the 
sense of smell. 

The attack itself is characterized by complete loss of con- 
sciousness, and is sometimes ushered in by an initial piercing 
cry or a noise like the roar of a wild beast which the patients 
emit at the moment of falling. This cry is by no means to be 
regarded as the expression of fear or surprise, as it does not 
occur until consciousness is lost and is a reflex act. It is ob- 
served in about fifty per cent of all cases, while in the remain- 
der it is either absent or replaced by tears. A tonic muscular 
contraction accompanies the cry. The head is at the moment 
of the fall drawn backward or to one side, the jaws are pressed 
together, the back is spasmodically curved, and the fingers are 
clenched over the adducted and flexed thumb. Respiration 
ceases, because the muscles performing the function take part 
in the spasm, and the face becomes discolored and cyanotic. 
A convulsive tremor runs over the whole body, and in the 
muscles of the face as well as in the rigid extremities twitch- 
ings begin to appear, which spread, and spare no part of the 
body. The head is violently knocked against the floor or the 
couch, the tongue rolled around in the mouth, protruded, per- 
haps, and retracted alternately, so that it is often injured by 
the teeth ; the eyeballs are deviated, the pupils dilated and in- 
active. Arms, legs, and trunk are now the seat of violent, ir- 
regular, rapidly changing jerkings. Corneal and skin reflexes 



536 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

are lost. The tendon reflexes can be obtained if the tetanic 
rigidity of the extremities allows it. The pulse is slightly 
quicker, the respiration greatly hurried. With each expira- 
tion the saliva, often foaming and mixed with the blood coming 
from the injured tongue, bursts forth and covers the lips. The 
temperature remains normal. In more protracted cases it may 
rise from one fifth to half a degree Fahrenheit. The involun- 
tary evacuation of urine and faeces, possibly also of semen, is 
not rare. In one case only have I seen the attack regularly 
associated at its onset with vomiting. 

Gradually the body becomes covered with sweat in conse- 
quence of the excessive muscular strain ; next, the convulsions 
lose some of their violence, the limbs gradually become less 
rigid, the cyanosis disappears, respiration, though it may still 
be difficult and snoring, becomes more regular, the coma 
abates and passes insensibly either into a deep, long sleep or 
gives place immediately to complete consciousness, so that in 
some cases the patient may in a few minutes again be in an 
apparently perfectly normal condition, without, however, hav- 
ing the slightest idea of what has been going on during the 
attack. 

We have said that the symptoms immediately preceding 
the attack present an endless variety of forms ; the same must 
be said of those that belong to the period following it. These 
" post-epileptic " phenomena may again be divided into psychi- 
cal and somatic. The psychical phenomena are very interest- 
ing, because they are not always of the same intensity, but 
may assume all gradations between a complete insanity (" post- 
epileptic insanity," post-epileptic moria, Samt) and a slight 
bewilderment. In the first case the patient has to be regarded 
as a madman, and must not be held responsible for his actions, 
not excluding any crime that he may commit at such times; 
in the latter he resembles a drunken man, who, although he 
later can not remember what has happened, will answer ques- 
tions if they are repeated often enough and in a sufficiently 
loud tone. Not uncommonly there exist immediately on 
waking up speech disturbances, either in the form of a motor 
or sensory aphasia, which lasts from a few minutes to several 
hours. Total aphasia following the attack has also come 
under my notice, and I have seen it persist for half an hour. 
The patient appeared to have regained consciousness pretty 
well, he understood, apparently, the questions which were 



EPILEPSY. 



537 



asked him, but was not able to answer them in any other 
way than by signs. Fiirstner has reported instances of post- 
epileptic stammering (Arch. f. Psych, und Nervenkrankheiten, 
1886, xvii, 2). 

Among the somatic post-epileptic phenomena there is, be- 
sides the difference in the size of the pupils, which is of some 
value for the diagnosis of nocturnal attacks occurring during 
sleep, a concentric contraction of the field of vision, which may 
last for twenty-four hours. Of this I have been able to con- 
vince myself several times positively. Further, there are cer- 
tain conditions of motor irritation, " cortical movements " 
(Rindenbewegungen of Zacher), which either consist of typi- 
cal clonic twitchings, or of choreoid or athetoid movements, 
and which may persist for hours. Contractures, occurring 
more frequently in the upper than in the lower extremities, 
usually on one side, have only been observed in exceptional 
cases (Lemoine, Deutsche med. Ztg., 1888, 20). Among the 
vaso-motor changes there are circumscribed reddenings which 
may occur symmetrically on both sides of the body in the 
most diverse places. Transient increase of the patellar reflex, 
transient albuminuria and violent vomiting are common after 
epileptic attacks. 

As to the time at which the attack may be expected, we 
may broadly say that there is not a moment in the life of the 
patient in which he can feel safe from them ; that any particu- 
lar time, either of the day or of the night, is especially danger- 
ous in this regard can not be maintained. This much only can 
be said, that in some individual cases the fits only occur during 
the night while the patient is in bed and asleep ; this so-called 
epilepsia nocturna possesses great practical importance, be- 
cause it may persist for a very long time unremarked and un- 
recognized, especially if the patient sleeps alone. If such be 
the case, the diagnosis can then only be made from certain 
characteristic signs observed in the morning — from the pain 
of the bitten tongue, the dull headache, the slight extravasa- 
tion of blood into the conjunctivae, or the unequal pupils {vid. 
supra). In one of my cases of nocturnal epilepsy there occurs 
after each attack a deep-red spot, the size of the palm of the 
hand, on the forehead, which does not begin to fade until one 
or two days have passed. For years the attacks may be con- 
fined to the night, and may go on without interfering to any 
extent with the patient's business and social life. Above all, 



538 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

he is not exposed to the usual injuries caused by the falls, but 
he never can feel absolutely certain that some time or other 
an attack may not occur during the day. These nocturnal 
fits are heralded by an irregular respiration, snoring, grunting, 
or moaning. Convulsions may not occur at all, but the whole 
body gets into a condition of tetanic rigidity which is followed 
by a relaxation of the muscles ; during the whole time the pa- 
tient does not awake, and has no consciousness of what has 
been going on. 

There are certain things which seem to exert an unfavora- 
ble influence upon the severity and the frequency of the fits, 
and against which the patient must be strictly and repeatedly 
cautioned. Of these the most important are sexual excite- 
ment, alcoholic excesses, psychical emotions, mental strain, 
etc. The indulgence in heavy indigestible food is harmful, 
especially in the evening. After imprudences of this kind 
the attacks may be found to come on more frequently, and at 
times when otherwise they would have undoubtedly not oc- 
curred. Whether the climate has anything to do with the 
fits we are not sure, and the idea of the supposed influence of 
the moon must be relegated to the domain of the unknown. 
It is interesting to note, however, that when an epileptic is 
taken ill with typhoid fever, pneumonia, facial neuralgia, etc., 
he may hope to enjoy immunity from the attacks as long as 
these diseases last. 

On the other hand, there are certain things which exert a 
favorable influence, either by aborting or preventing for cer- 
tain periods the occurrence of the attacks. How these factors 
work is quite inexplicable. Among the former may be men- 
tioned the application of a tight bandage or strap to the part 
of the body — e. g., the finger or hand — in which the motor 
aura occurs ; to the latter belongs frequent epistaxis, as I have 
repeatedly had occasion to observe ; if it was profuse it seemed 
to produce an intermission in the occurrence of the attacks 
which lasted for a relatively long time. 

Besides the classical attack which we have just described, 
and which is known as "grand mal," there occur rudimentary 
abortive attacks, as it were, which have received the name 
"petit Dial!' Of this latter kind there exist countless varieties. 
There may be nothing more than a momentary vertigo, with- 
out any loss of consciousness ; this is then termed epileptic 
vertigo ; or in place of or following this there may be a short 



EPILEPSY. 



539 



loss of consciousness, lasting but a few seconds, the "absence" 
of the French writers, of the onset and the duration of which 
the patient is unable to give any account. An individual may 
in the middle of any kind of occupation — speaking, eating, 
reading, and so forth — suddenly stop what he is doing ; for an 
instant he stares vacantly before him, remains as he is, standing 
or sitting, and immediately after the " attack " resumes his oc- 
cupation as if nothing had happened ; the unfinished sentence 
is after a short pause completed, the spoon which was ready 
to bring the food to the mouth after a short stop reaches its 
goal. If an "absence" occurs to the patient on the street 
when he is out walking, he keeps on mechanically, loses his 
way perhaps, and only finds it again when consciousness re- 
turns. The instances in which such periods take in a much 
longer time, during which the patients undertake voyages, 
spend money, transact business of which they are not con- 
scious later, or do things which are against their intention and 
entail disagreeable consequences, must also be looked upon as 
coming under the head of epilepsy. They are undoubtedly 
rare, and up to this time have only been carefully observed by 
French physicians, more especially by Charcot (" automatisme 
ambulatoire "). Insignificant as petit mal may seem, it often 
has a very deleterious effect upon the general condition of the 
patient, especially upon the mind ; we should be cautious, 
therefore, with our prognosis. 

There are still other seizures in which typical convulsions 
do not occur, but where the patient suddenly begins to walk 
first forward, then backward, or to run around in a circle 
(" mouvements de manege "), or spin round and round, or he 
may rush out of his house and run for long distances without 
knowing why or whither. This form, which has been de- 
scribed by Bourneville, Ladame, and others, is called " run- 
ning epilepsy," epilepsia procursiva. It often appears in 
childhood, and later gives place to the usual classical attacks. 
Its frequent combination with moral insanity is interesting. 
Anatomical changes have not been found in the cases which 
came to autopsy up to the present. 

Again, instead of the convulsive attacks, we may have from 
time to time transient psychical disturbances, which consist 
either of states of excitement or depression ; in such instances 
we speak of "epileptic equivalents" (Samt). We must leave 
to the psychiatrists the task of investigating their cause and 



54Q 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



their significance. From a medico-legal point of view these 
puzzling conditions possess great interest. 

About the frequency of the paroxysms no definite state- 
ment is possible. There are people who during their whole 
life have not more than one, two, three, six, or ten attacks, and 
again there are others in whom they recur once a week or still 
more frequently. Sometimes there are certain periods in 
which they increase in frequency, and others of months or 
years during which only an occasional attack occurs. In rare 
instances, in periods of the former kind, the fits may succeed 
each other so closely that there may be one or even many 
every day. Before the patient has had time to regain his full 
consciousness another attack looms up. This is what we call 
the status epilepticus, etat de vial. The temperature may rise 
steadily for from three to eight days as much as 5 to 7 F., so 
that it may reach 104 or 106 F. If, then, in the intervals 
consciousness does not become fully restored, but the patient 
remains dull and bewildered, there is very great danger that 
death may occur during the status epilepticus, and the friends 
should be made acquainted with the seriousness of the situa- 
tion. Only in exceptional cases does recovery take place and 
the temperature fall to normal again (Witkowski, Ueber epi- 
leptisches Fieber u. s. w., Berliner klin. Wochenschr., 1886, 
xxxiii, 43, 44). 

Course. — The course of the disease, the general condition 
of the patient in the intervals between the attacks, the influ- 
ence of the attacks upon the mind and body — all these may 
present great variations. 

The course is very chronic and the disease lasts in most 
cases years and tens of years. Frequently the patient is sub- 
ject to the affection during his whole life. The earlier the first 
attacks make their appearance the less chance is there of their 
complete disappearance. In some cases of " late epilepsy," 
" e'pilcpsie tardive" in which the affection does not begin until 
late in life, it may happen that the attacks completely cease as 
unexpectedly as they came on. Still, a course so favorable as 
this is rare and can never be predicted with certainty. If the 
disease has set in in early childhood, the influence of the peri- 
od of puberty is generally very marked. The attacks become 
more frequent, and in women the increase in number is ob- 
served every month at the time of the menses until the time of 
the menopause. Pregnancy has little influence on the attacks, 



EPILEPSY. 



541 



according to my own experience ; sometimes it appeared as if 
shortly after conception the number of fits was considerably 
lessened, while in other women there seemed to be no change. 

The general condition in the intervals between the attacks 
is by no means the same in all cases. In some, fortunately not 
rare cases, the paroxysms do not cause any bad effects for 
years and nothing morbid can be discovered. The mental fac- 
ulties develop normally or, if already developed, remain good. 
The disposition is cheerful, social intercourse is enjoyed, as 
there is nothing in the bodily condition to interfere with such 
pleasures. The presence of epilepsy does not necessarily pre- 
vent the full development of a genius, as is proved by the uni- 
versally quoted historical examples of Cassar, Alexander the 
Great, Rousseau, Napoleon I, and others. 

In other instances the general condition in the intervals 
leaves much to be desired, and as a rule it is the psychical part 
of the man which suffers most unpleasantly. Either the dispo- 
sition of the patient is changed for the worse, so that he is 
easily excited, irascible, suspicious, and peevish, unsociable, 
and disagreeable to those around him, or the mental faculties 
suffer, he becomes dull, slow in grasping ideas, indifferent, anx- 
ious, abstracted, and so unreliable in his work that he is no 
longer able to fulfill his duties as a man of business and as a 
good citizen. 

In such cases we are sometimes able to note bodily defects, 
as, for example, abnormities in the formation of the skull, in 
the form of the auricle, in the condition and arrangement of 
the teeth, etc. Such " signs of degeneration," however, are 
frequently not present. 

The final issue of the disease is almost always the same. 
The patient remains an epileptic all his life, from time to time 
having attacks, and finally dies from some intercurrent malady. 
The mental faculties may remain throughout, on the whole, 
good and the capacity of the patient for following his calling 
be retained. In other instances the mind becomes gradually 
impaired, so as to necessitate the transference of the patient to 
an institution, or again, in very exceptional cases, there may be 
complete recovery or, at any rate, so marked a decrease in the 
frequency of the attacks that the patient may well regard him- 
self as cured. This cure may come about spontaneously or 
may be caused by some unexpected psychical emotion, par- 
ticularly a fright. However, we should beware of being too 



542 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



precipitate in calling a patient " well," because now and then 
even after intermissions of , years an attack may again make its 
appearance. 

Death rarely ever occurs during an attack, but indirectly 
the paroxysms may cause a fatal issue. The patient may re- 
ceive during his fits serious wounds, or may fall upon his face 
and be suffocated, or fall into the water and be drowned. The 
average life of epileptics is considerably shorter than that of 
other persons. 

./Etiology. — Although we may be able to mention some fac- 
tors which seem to have something to do with the occurrence 
of the disease, we are unable even to hazard a conjecture in 
what manner in a given case this or that factor can evoke an 
attack, more particularly the first attack ; but our ignorance is 
not surprising if we consider that we have never as yet been 
able to find any anatomical changes of the brain associated 
with this disease. 

It has been the habit of most writers to distinguish predis- 
posing or general from exciting or special causes, and among 
the former heredity has been given the first place. There is 
no doubt but that hereditary neuropathic tendencies increase 
the susceptibility to nervous diseases in general, and certainly 
to epilepsy ; but this heredity alone does not suffice to make of 
an otherwise healthy individual an epileptic. For this usually 
an additional cause is needed, as, for instance, syphilis. If an 
individual with hereditary tendencies acquires syphilis, he is 
more likely to become epileptic — that is, to suffer from a genu- 
ine epilepsy which is neither preceded nor followed by any ap- 
preciable anatomical changes either in the brain or in its ves- 
sels — than a person infected with the same disease but burdened 
with no family history. Of course there are other cases, too, 
of cerebral syphilis with the characteristic arterial disease in 
which epileptic attacks occur entirely independently of any he- 
redity (cf. Barbier, De Tepilepsie syphilitique et de son diagnose 
differentiel avec l'epilepsie vulgaire. These de Paris, 1885). 
Important, therefore, as heredity may be, it is by itself not suf- 
ficient to constitute a cause of epilepsy. The manner, of course, 
in which the tendencies were acquired is also irrelevant, and 
the question whether the father or mother or both were given 
to alcoholism, and whether both or either of the two were in- 
toxicated at the moment of generation of the child, has no sig- 
nificance. Notwithstanding the relative frequency with which 



EPILEPSY. 



543 



epilepsy occurs, the number of cases would be much larger if 
either of these factors could have any decided action upon the 
appearance of the disease. 

Age and sex seem to have little influence in this connection. 
Although it is true that in the majority of cases the disease af- 
fects individuals in the first half of their lives, more especially 
between the ages of ten and twenty, it may begin much later, 
after the age of forty or fifty. Indeed, cases in which the first 
attack made its appearance between the sixtieth and the seven- 
tieth year have been recorded. 

With regard to sex, it has been noted that during the 
period of puberty, between twelve and sixteen, more girls 
than boys become epileptic ; if, however, the average of all 
cases is taken, the difference between the numbers in the two 
sexes is very slight, and in early childhood, from the fourth to 
the seventh year, it is nil, the cases being equally distributed 
between the two sexes. 

Among the exciting causes there is in reality only one, the 
mode of action of which we are able to understand to any ex- 
tent, and that is traumatism, and more especially injuries to 
the head. It may happen that a person, previously perfectly 
well, is taken with an epileptic fit after a fall or a blow upon 
the head ; but here we must distinguish between injuries 
which cause a lesion of the brain cortex and those which do 
not ; in the former case the lesions become the direct cause of 
the attacks, and we have not a genuine epilepsy, which we 
said was one based upon no appreciable anatomical changes, 
and which, therefore, only occurs if the brain be uninjured. 
We must carefully examine the scalp, and overlook no scar, 
however trivial, because any one may be the cause of the epi- 
lepsy. The probability becomes a certainty if the cicatrix is 
adherent to the bone beneath it and is painful to the touch, 
and if it is possible by firm pressure to bring about an attack ; 
in this case, as we shall insist upon later, excision is indicated. 

The attack which occurs in consequence of this pain is a 
reflex act, and this kind of epilepsy we call " reflex epilepsy." 
Such reflex attacks may also be caused by painful cicatrices on 
the peripheral nerves at any point of the body, or where there 
exist ulcerative processes — for instance, of the finger nails. In 
one of my patients it was possible every time to produce an 
attack by pressure upon the diseased matrix of the nail, the 
same thing occurring also when he accidentally struck it 



544 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

against anything. The amputation of the terminal phalanx 
was followed by complete recovery after all other measures 
had proved fruitless. In a similar manner polypi of the ear 
(" ear epilepsy "), inflammatory processes in the ear, intestinal 
parasites, an incarcerated hernia — finally, also diseases of the 
sexual organs, in the male as well as in the female, may give 
rise to epileptic attacks. If, after a heavy indigestible meal at 
night, the patient is for the first time seized with an epileptic 
fit, as by no means uncommonly happens, the attack has also 
to be looked upon as reflex in nature. 

It is well known and beyond question that psychical influ- 
ences may become the direct cause of epileptic seizures, al- 
though how and why we do not understand. The most im- 
portant of these is fright, which in numerous instances has 
been known to be the cause of the disease ; but how shall we 
explain the instances in which persons perfectly healthy up to 
that time suddenly become epileptic in consequence of the ex- 
citement of a shocking spectacle or of a dangerous situation — 
e. g., an assault by robbers or the menacing appearance of a 
fierce dog — and then remain so during their whole life in spite 
of all treatment? What changes go on in the brain in such a 
short time, and of what nature can they be that they can per- 
sist for many years ? This question, with which we are unfor- 
tunately too frequently confronted, presents difficulties which 
appear insurmountable. 

Closely related is the influence which the frequent sight of 
epileptic convulsions exerts upon healthy individuals, an influ- 
ence which can hardly be accounted for by fright, but which 
is to be referred to a peculiar, most remarkable imitative im- 
pulse. In the royal prison of Breslau I have known thirteen 
of a large number of female inmates who were working to- 
gether in a room become epileptic a short time after another 
prisoner, who had been suffering from epilepsy for years, had 
been brought into the same ward. The prognosis in this imi- 
tation epilepsy we would hasten to say is the most favorable, 
far better even than in " fright epilepsy." 

Lastly, we would call attention to the fact that epilepsy may 
be caused by certain substances which are taken into the sys- 
tem, whether as food or for the sake of their agreeable effects, 
or, again, as medicines, when used in large quantities or for 
too long a time. Among the first we have alcohol, absinthe, 
and so forth, then fungi (mushrooms), certain spices (Cayenne 



EPILEPSY. 



545 



pepper and paprika) ; to the second belong all narcotics, more 
especially, as we have recently learned, cocaine. The " cocaine 
epilepsy " has been described by Heimann (Deutsch. med. 
Wochenschr., 1889, 12). Under certain circumstances other 
medicines — e. g., antipyrine — may act as poisons and lead to 
epileptic attacks (cf. Tuczek, Die Antipyrinepilepsie, Berl. klin. 
Wochenschr., 1889, 17). In view of the extensive use which 
this last-mentioned drug has obtained in a short time, and the 
popularity which it enjoys, and on account of which it is used 
in all possible kinds of diseases, however different from each 
other, this observation must be regarded as possessing great 
practical importance. 

Pathogenesis. — The pathogenesis of epilepsy is totally ob- 
scure ; although we know from the experiments of Kussmaul 
and Tenner that the source of the attacks must be sought for 
in the brain, the exact seat of the disease is not known. Since 
the work of Schroder van der Kolk special attention has been 
given to the medulla oblongata, and the discovery by Noth- 
nagel of a " spasm centre " in the pons seemed greatly to sup- 
port the " bulbar theory," but of late years this has more and 
more fallen into discredit, and it is now the brain cortex which 
is regarded as the starting point of the convulsions (Hitzig, Al- 
bertoni, Franck et Pitres, P. Rosenbach). For a long time the 
motor area was thought to be the only region concerned, but 
recently Unverricht, who, with his convincing experiments on 
animals, has proved himself the most successful defender of the 
cortical theory (after extirpation of an area in the cortex he 
found that he could not obtain spasms in the muscle groups 
corresponding to it) has shown that excitation of the posterior 
cortical regions is also capable of producing an attack, hence 
that these too possess epileptogenic properties, and that irri- 
tation of the same may by extension of the stimulus to the 
motor area give rise to general convulsions (Deutsch. Archiv 
f. klin. Med., 1888, 44, 1). 

Binswanger agrees that in the lateral portions of the floor 
of the fourth ventricle there are points the stimulation of 
which gives rise to spasms, which, however, he considers to 
be of a reflex nature, and assumes the reflex centres to be sit- 
uated in the dorsal half of the pons. According to his opinion, 
these represent, as it were, a collecting station for the centres 
of the spinal cord, and can not, in the physiological sense, be 
termed " spasm centres." He maintains that we never can 
35 



546 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

succeed by electrical or mechanical stimulation of the pons in 
producing real epileptic attacks. 

However probable an association of the cortex with the 
appearance of symptoms of motor irritation may seem, such 
an association is far from explaining the increased salivary 
secretion, the involuntary evacuation of the bladder, the in- 
crease in the frequency of the respirations, etc., and we must 
for the present leave the question open whether or not such 
phenomena depend upon some influence acting on certain cen- 
tres in the brain and spinal cord, the situation and function of 
which we do not as yet know. The question raised by Ziehen 
as to the significance of the subcortical ganglia in the causa- 
tion of an epileptic attack deserves to be looked into more 
closely ; for the present only this seems certain, viz., that (in 
dogs) the clonic part of the convulsive movements produced 
by stimulation of the cortex is connected with the cortex itself, 
while the tonic and the running movements seem to be of sub- 
cortical origin (XIII. Wanderversammlung siiddeutscher Neu- 
rologen. Archiv f. Psych., 1889, xx, 3, page 584). 

Symptomatic Epilepsy. — As we said at the beginning of 
this chapter, there exists not only a " genuine," but also a so- 
called " symptomatic epilepsy," which does not constitute a 
clinical unit, but which comprises a number of different affec- 
tions based upon various anatomical changes. The appearance 
of convulsions, during which consciousness can be retained, 
may be regarded as their chief common characteristic. 

Here we must first call attention to that form of cortical 
lesion upon which we have touched already on page 184. It 
is clinically characterized by convulsions, which are sometimes 
confined to one arm or one leg, in general to a part only of the 
body, and has, therefore, received the name, very inappro- 
priate, indeed, of partial epilepsy, or, after its anatomical seat, 
cortical epilepsy, or, again, after the author who first described 
it, Jacksonian epilepsy. The seizures are distinguished from 
the classical epileptic fits by the fact that consciousness is 
maintained, a circumstance which, of course, makes the two 
clinical pictures quite different. An aura may occur, it is true, 
in this form also, so that the patient knows when the convul- 
sions are going to appear, either from a slight twitching in the 
fingers or toes or from feelings of formication, etc., signs which 
appear only in the affected extremity ; but all other symp- 



EPILEPSY. 



547 



toms, the cry, the biting of the tongue, the fall, and so forth, 
are absent. The patient sees and watches the twitching of his 
extremity, and may at the same time" complain of considerable 
pain. He himself holds the limb or has it held by others, so as 
to avoid as much as possible any injury to it. After the attack 
he feels weak and exhausted, but only on account of the in- 
creased muscular work. Headache and all the various " post- 
epileptic " phenomena are wanting, or if they occasionally do 
occur, have no connection with the attack, and have, therefore, 
no claim to be reckoned under this head. 

The degree, duration, and frequency of the attacks are ex- 
tremely variable ; sometimes they consist only of a more or 
less marked twitching, which appears in the affected extrem- 
ity ; sometimes there are shaking movements which can attain 
to so high a degree that the bed, on which the patient lies, is 
also shaken under him, and he anxiously calls for some one to 
come and hold him still. If considerable pain come on during 
the movements, it usually continues after the attacks and is a 
great source of trouble to the patient in addition to the motor 
weakness in the affected extremity. The duration also of the 
attacks varies : I have seen some which were over in from 
fifteen seconds to a minute ; on the other hand, cases have 
come under my notice in which a quarter, a half, or even an 
hour was taken up by the involuntary movements. If these 
attacks recur often — twice, three times* or six times a day — the 
condition of the patient is most distressing, and the partial 
epilepsy can do more to ruin his life than the classical form 
would ever have done. In other instances the attacks are so 
few and far between that the patient almost forgets one before 
he has another, as many months may have passed. The whole 
course of the disease is eminently chronic ; the patient may 
suffer from the affection for tens of years without presenting 
any other symptoms. Death is finally caused by an extension 
of the brain lesion or by an intercurrent disease. Pitres has 
called attention to the fact that in this form also " equivalents " 
may occur (Revue de m6d., 1888, viii), and has pointed out 
that they may be sensory or psychical. The former have been 
called by Charcot Vepilepsie partielle sensitive (Lecons du Mardi 
a la Salpetriere, 1889, pages 20 and 368); in the latter we have 
to deal with hallucinations of sight, hearing, and smell, which 
occur paroxysmally without the appearance of any decided 
symptoms of motor irritation. 



548 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



A peculiar kind of epilepsy, which is said only to occur in 
heart disease, has been described by Lemoine (De l'epilepsie 
d'origine cardiaque, Revue de med., vii, May 5, 1887), yet 
since the connection is not absolutely proved, and since, more- 
over, the attacks themselves present no peculiarities of their 
own, we shall limit ourselves to saying that they disappeared 
under the administration of digitalis. 

Lately von Jaksch (Zeitschr. f. klin. Med., 1885, x, 4) has 
shown that epileptic attacks may be produced by auto-intoxica- 
tion, not only by urea, but in a similar way also by acetone. In 
cases of "epilepsia acetonica" large amounts of acetone were 
found in the urine, which besides contained neither sugar nor 
albumen. The physiological connection between the occur- 
rence of acetone in large quantities in the urine and epilepti- 
form attacks is not as yet fully established, nor do we know 
how poisons — for instance, lead — introduced into the organism 
from outside are able to produce such attacks ; as a matter 
of fact, however, lead workers suffer so frequently from 
epilepsy that we are justified in assuming the existence of a 
definite " epilepsia saturnina" (Hirt, Krankheiten der Arbeiter, 
iii, 49). 

Briefly, epileptic attacks may occur as a symptom also in 
meningitis, dementia paralytica, during delirium tremens, in 
sclerotic processes, more especially frequently in sclerosis of 
the cornu Ammonis. They may be associated with tumors, 
hydrocephalus, or abscess of the brain, in which cases they are 
the result of the increased intracranial pressure, as we have 
pointed out above. From what has been said in this and in 
previous chapters it will be understood that these and the so- 
called epileptiform attacks above mentioned have in all proba- 
bility nothing to do with the genuine classical epilepsy. 

Diagnosis. — We can well understand, then, how cautious 
we must be in our diagnosis. Only after repeated and careful 
examinations, after which we are able to exclude organic brain 
diseases, abnormities in metabolism, in consequence of which 
abnormal or poisonous substances occur in the urine (urea, 
sugar, acetone), are we justified in making the diagnosis of 
genuine epilepsy. The skin and tendon reflexes should always 
be carefully examined. Sometimes, from the absence of the 
abdominal or cremasteric reflex, or from a unilateral increase 
of the patellar reflex, we may be able to diagnosticate an 



EPILEPSY. 



549 



organic brain trouble when we otherwise, without any inquiry 
into the condition of the reflexes, might have regarded the case 
as one of genuine epilepsy. 

The conditions for which the epileptic attack itself or the 
coma following it could be mistaken have been discussed in 
our account of cerebral hemorrhage. We only need add here 
that cortical epilepsy may be simulated by ursemic attacks if 
the latter are confined to one side. Chauffard (De l'uremie 
convulsive a forme de l'epilepsie Jacksonienne, Arch, gener. de 
med., July, 1887) has called attention to this. Hysterical at- 
tacks may bear a striking resemblance to those of Jacksonian 
epilepsy ; in such cases the recognition of other hysterical 
symptoms should prevent any diagnostic errors. Mendel has 
repeatedly observed that progressive paralysis of the insane 
may commence with attacks of this kind. The foci which 
were found at the autopsy were in every case situated in the 
right psycho-motor region, and the paralytic speech disturb- 
ance did not occur until late in the disease, whereas usually 
it is one of the earliest symptoms. The possibility, finally, of 
confounding epilepsy with eclampsia we shall discuss shortly. 

Quite frequently we meet with malingerers who, for some 
reason or other, feign epilepsy. The situations in which the 
simulation of this disease would be likely to be advantageous 
to the deceiver are quite numerous, and it would be impossible 
to enter into the consideration of them here ; we will only men- 
tion that epileptics are dispensed from military service, good 
grounds enough for many to sham this disease. The more 
cunning the malingerer the more perfect will be the attack, 
not excluding the foaming of the mouth (made by soap) and 
the (not very deep) wounds of the tongue ; there will be con- 
vulsions and the (feigned) loss of consciousness is possibly pro- 
longed more than is necessary ; if the rogue has courage 
enough he will not betray himself either by a reflex motion of 
defense, or even by the slightest twitching, if hot sealing wax 
is, as a test, dropped on his chest. Under certain circum- 
stances it may be extremely difficult to unmask the fraud ; it 
might, indeed, be impossible, did we not know one reflex over 
which the will has no power, namely, the pupillary reaction to 
light, which in the epileptic is lost, in the malingerer naturally 
is retained. In doubtful cases, therefore, this reflex has to be 
carefully observed, and the further measures should depend 
upon its condition. 



55o 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



Treatment. — The treatment of epilepsy confirms the old 
experience that the greater the number of remedies which 
become known and are recommended for a disease, the more 
difficult and uncertain becomes the cure. In the course of 
centuries such an array of medicaments have been recom- 
mended to combat this disease that there is hardly a drug in 
the shops which has not at one time or another been regarded 
and praised as an infallible " specific." Unfortunately, all these 
claims have been proved to be false. We are to-day as little 
in a position to cure epilepsy as we were one or five centuries 
ago. Only by the discovery of some causes which may pro- 
duce epilepsy, the removal of which lies in our power, has any 
progress been made in the treatment of the disease. This more 
particularly applies to the above-mentioned reflex epilepsies. 
Here a cure is possible — nay, we may say even certain — if we 
are able to remove the cause. To discover it must be the phy- 
sician's aim. Sometimes it consists of a bone splinter which is 
left after an injury to irritate the cortex, in which case a cure 
will invariably be effected by the operation of trephining for 
the removal of the splinter. In other instances painful cica- 
trices have to be excised or affections of the intestinal tract or 
the sexual apparatus treated. In children the natural openings 
of the body have to be examined for the possible presence of 
a foreign body, the removal of which would then be absolutely 
necessary. 

Such are the favorable cases in which it is in the power of 
the physician to bring about a cure. Unfortunately, their 
number is not great. In the largest majority of instances we 
are not able to find any cause, the removal of which would re- 
move also the disease ; but to-day, as centuries ago, we are re- 
duced to the sad necessity of trying all sorts of remedies, trust- 
ing to good luck that at some time we may hit upon one which 
is truly efficacious. 

Among the internal medicines the so-called specifics possess 
an interest purely historical ; from artemisia (in hot beer, 10 to 
20 grm. at a dose — grs. 1 50 to 300) and Valeriana down to squilla, 
gratiola, sedum, cardamine, and hellebore, many herbs have 
been lauded as effectual. Asafcetida, castoreum, and camphor 
have been recommended, although no better results have been 
obtained from them than from silver nitrate, ammonio-sulphate 
of copper, and arsenic. A great sensation was created by Meg- 
lin's pills, which, in addition to zincum album contained hyos- 



EPILEPSY. 



551 



cyamus. Some have sworn by oxide of zinc, and Herpin, for 
instance, claimed that out of forty-two cases he cured twenty- 
eight with it. To unprejudiced judges who continued their 
observations for a sufficiently long time these " cures " could 
not hold their ground. They proved to be deceptive, and we 
were as helpless as before. Recourse was also had to narcot- 
ics, and much was hoped from the action first of opium and 
later of ether and chloroform. It is true that here and there 
an attack has been cut short by inhalations of the latter, but 
that is all. It is not to be wondered at that under such cir- 
cumstances secret remedies were used to a tremendous extent; 
and to what a pitch the humbug and impudence were car- 
ried may be seen from the composition of some such remedies, 
for instance, the epilepsy powder of the Institute for Deacon- 
esses in Dresden, which consisted of charred bone of magpies 
which had to be shot at some time during the twelve nights 
following Christmas, and again from the epilepsy powder of 
Wepler, which was nothing but charred and pulverized hemp 
thread (cf. Richter, Das Geheimmittelunwesen, Leipzig, 1872, 
pages 15-16). 

A new era in the treatment of epilepsy — that is, of the at- 
tacks — was initiated when Locock in 1853 recommended bro- 
mide of potassium, which obtained a wide acceptation through 
the efforts of Legrand du Saulle. Its power of diminishing the 
reflex irritability and of lowering the blood pressure in the 
brain has placed it first among the antispasmodics, and to-day 
it has to be regarded as the best and most important medicine 
in the treatment of epilepsy. In order not to be disappointed, 
however, in our expectations, it is necessary that we should be 
familiar with the proper regulation of the dose and with cer- 
tain unpleasant effects which are apt to arise in the course of 
the treatment. The small and moderate doses of 0.5 to 4 grm. 
a day (grs. viij to 3 j) formerly used are generally ineffectual. 
It is necessary to employ much larger amounts, which are 
best given in one dose. It is, moreover, better to combine the 
three bromides, viz., the bromides of potassium, sodium, and 
ammonium, in equal parts than to give bromide of potassium 
alone. The minimum daily dose for adults in cases of pro- 
nounced epilepsy is eight grammes (3ij), and we should fol- 
low Mendel, who advises that it should be taken in valerian 
tea immediately before going to bed (potassium bromide, am- 
monium bromide, aa 2.5 (grs. xxxviij); sodii bromidi, 3.0 (grs. 



552 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



xlv). For children and young people up to sixteen years of 
age the daily dose should be half a gramme (grs. vij) for every 
year. If the two drachms are not sufficient — that is, if an at- 
tack still occurs now and then — the dose may be increased to 
ten or twelve grammes ( 3 ijss. to 3 iij), and this continued until 
four or five hundred grammes or from six to nine ounces are 
taken. 

In this way I have treated hundreds of epileptics in private 
as well as in dispensary and hospital practice and have let slip 
no opportunity for observing the action of the bromides. This 
action is by no means the same in all cases. There are people 
in whom an idiosyncrasy against the medicine rapidly devel-) 
ops, so that it is impossible for them to take it any more. It 
nauseates them and may cause vomiting, and after repeated 
unsuccessful trials to resume the treatment we have to discon- 
tinue it entirely. In other instances the desired effect on the 
attacks may show itself ; but after a few weeks the patient be- 
gins to complain of general bodily and mental feebleness, a 
constant desire to sleep, some loss of memory, and other symp- 
toms, so that the dose has to be diminished. At the same time, 
sometimes without these symptoms, an eruption on the skin 
appears, more especially an extensive, obstinate acne distributed 
over face, trunk, and extremities, which is most distressing, 
especially to young female patients. I have seen this eruption 
particularly after the prolonged use of small doses, and have 
also seen it disappear comparatively rapidly under the use of 
mild laxatives and the administration of arsenic in the form of 
Fowler's solution. Finally, cases come under our notice in 
which bromide, no matter in what form or dose it be given, is 
entirely without effect. The attacks occur just as they did 
previous to the administration of it. Here we have, of course, 
again to suspend the treatment, more especially if symptoms of 
intoxication appear in addition to the continuance of the fits. 
If we wish to express the effects of bromide in epilepsy by 
percentages, we could say that in about ninety per cent of all 
cases the paroxysms diminish in number and violence, that in 
about as many signs of bromism appear which render neces- 
sary a diminution of the dose or a gradual suspension of the 
medicine. In from two to three per cent of all cases bromide 
is borne so badly that it has very early to be discontinued. 

If it is established beyond doubt that the bromides exert a 
favorable action, we must insist upon their prolonged use for 



EPILEPSY. 



553 



months and years. To add some variety to the treatment they 
may be combined with belladonna and pills may be ordered 
which contain both. If every evening two centigrammes (gr. 
y 3 ) of belladonna and two grammes (grs. xxx) of bromide are 
given, about the same results are obtained as with eight 
grammes (3ij) of bromide alone. [IJ Extr. bellad., 0.5 (grs. 
vijss.) ; pot. brom., sodii brom., ammonii brom., aa 15 (3SS. 
circ.) ; pulv. et succ. liq., aa q. s. ut. f. pil. No. 50. Signa : One 
to two pills in the evening.] When the action of the bromide 
gradually becomes lessened owing to the establishment of a 
tolerance, the administration of belladonna is also indicated, 
and it may then be given in the form of Trousseau's pills. (1$ 
Extr. bell., Fol. bell., aa 1.0 (grs. xv), succ. q. s. ut. f. pil. No. 100. 
Signa : One to two, later three to four, or even six pills, in the 
evening.) 

Stevenson, in the Medical Press and Circular, 1888, 24, 10, 
has recommended bromide of camphor very warmly (camph. 
brom., 0.6 — grs. ix — at a dose several times a day). Our expe- 
rience with this drug does not agree with his. We have never 
obtained any lasting effect with it. 

Compared with bromide and belladonna, which, according 
to our opinion, are the only reliable drugs to be used in the in- 
ternal treatment of epilepsy, the medicaments which have been 
recommended of late years — curare, considered to be effectual 
by Bourneville, antipyrine by Beaumetz, tinct. simulo (the 
fruit of Capparis coriaced), which has been used by White — do 
not play any important role, and only deserve a trial in desper- 
ate cases. On the other hand, amylene hydrate, recommended 
by Wildermuth (cf. lit.), must be given a trial in cases of dis- 
tressing bromism or if the attacks increase to an alarming ex- 
tent. The watery solution of Kahlbaum's preparation, in the 
proportion of one to ten, is the best to use in doses of from 
twenty to forty grammes ( 3 v to 3 x) — i. e., two to four 
grammes (3ss. to 3j) of the drug itself. It may be given in 
wine or water or in a glass of beer, well shaken up, and from 
five to eight grammes of the drug (3jss. to 3 ij) may thus be 
used daily. 

Surgical interference has also been resorted to, at first with 
the view of influencing or diminishing the amount of blood in 
the brain. Several times the carotids have been ligated, and 
two cases thus treated were reported as completely cured 
(Hasse, Krankheiten des Nervensystems, page 297). Owing to 



554 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



the great difficulties of the operation and the great responsi- 
bility which the physician takes upon himself, this measure 
will only in exceptional cases be made use of. With bleeding, 
strong revulsives to the skin, such as Autenrieth's ointment to 
the shaved head, moxas, setons, blisters, and purgatives, possi- 
bly the same results can be obtained. 

Quite recently both vertebral arteries have been ligated 
(von Baracz, cf. lit.). In my clinic the ligation of one verte- 
bral, the right, was performed several months ago by Janicke 
without any noticeable effect upon the frequency or the sever- 
ity of the attacks ; hence the patient was not willing to submit 
to the ligation of the other. The operative treatment of trau- 
matic epilepsy aims at the removal of bone splinters which 
press upon and injure the brain cortex ; but the operation 
should only be performed, as von Bergmann holds, if the con- 
vulsions constantly occur in the same groups of muscles and 
extend in a characteristic manner, or if transient hemipareses 
occur. At the operation the affected area of the cortex has to 
be carefully excised. If the attack begins like a flash without 
an aura and is associated with opisthotonus, etc., operative 
measures are contraindicated. 

Marshall Hall's advice to perform tracheotomy, on the 
ground that the spasm of the glottis is productive of the as- 
phyxia and the clonic spasm, is purely and entirely of histor- 
ical interest. The operation has been performed several times 
without, of course, the least benefit to the patient. The same 
may be said of the cauterization of the glottis with nitrate of 
silver, suggested by Brown-Sequard, which has been justly 
condemned in such cases. 

In connection with the surgical treatment we should men- 
tion the application of strips of cantharidal plaster around the 
forearm or lower leg in which the motor or sensory aura oc- 
curs. Only when the aura constantly appears in the same 
member can any success be expected from this measure, which 
has been recommended by Buzzard. The plasters must re- 
main on for a considerable time. Following the advice of Buz- 
zard, I have ordered the application of these plasters in some 
cases, without, however, having been able to see any good re- 
sults. In one instance of partial epilepsy a transfer was pro- 
duced by the application of the plaster (Hirt, Neurol. Central- 
blatt, 1884, 0- 

Finally, we can hardly be surprised that attempts have 



EPILEPSY. ^t 

been made to combat epilepsy by electrical treatment. Un- 
fortunately, the results with this have been even less encourag- 
ing than those from internal medication. Neither the attacks 
themselves nor the so-called " epileptic change in the brain," 
the nature of which, as we have above stated, is still obscure, 
have been influenced by it in any way. The constant current 
was employed and the sympathetic galvanized by passing the 
current from one mastoid process to the other, and attempts 
were made to influence the cerebral hemispheres, and more 
especially the motor regions, according to Erb's method (Erb, 
Handbuch der Electrotherapie, page 581). In other cases the 
current was passed through the lobes of the thyroid gland, as 
Sighicelli (Rive, sperim. di freniatr., 1888, vol. xiii, 3) has quite 
recently done, but in none of them could any lasting success 
be remarked. No better results have been obtained with the 
faradic current in all its different modes of application. 

Although with all our treatment we are practically power- 
less against the disease, it would be very wrong to assume that 
to the epileptic the physician can be of no use and can not im- 
prove his condition in any way. On the contrary, there is 
hardly another class of patients affected with nervous diseases 
who require so much a physician's advice, and hardly another 
class who have to be so carefully watched by him. Above all, 
attention has to be paid to the general condition. The bowels 
must be kept regular and the skin and muscles stimulated to 
their proper activity by appropriate cold-water treatment and 
home gymnastics. The patient should constantly be warned 
against every kind of excess. Too large a supper, a few glasses 
of wine or beer taken too quickly, any indigestible food, ex- 
cesses in Verier e — all these may give rise to an attack, the con- 
sequences of which are incalculable. To guard against these, 
therefore — in other words, to employ prophylactic measures- 
is the chief task of the physician who is taking charge of an 
epileptic. Besides this, the bromides, or, if these are not suit- 
able, the next best treatment, should be begun. Finally, care 
must be taken that the patient does not hurt himself during the 
fit, and against this he should be protected as well as possible. 
All tight clothing must be removed and all ordinary emergen- 
cies provided for. A regular treatment of the attack itself 
we do not possess, and all attempts to cut it short should be 
avoided. Even inhalations of amyl nitrite, which O. Berger 
suggests, chloroform, and similar remedies are only allowable 



556 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

if administered with the greatest caution, and it would be bet- 
ter still to discard them entirely. 

Note. — Eclampsia is one of those terms which up to the 
present do not convey to our minds any clearly defined clinical 
or pathological picture. It is a term under which are compre- 
hended the most heterogeneous conditions which have not the 
least connection with each other. If a woman during preg- 
nancy or during parturition without any appreciable cause 
loses consciousness and falls into convulsions, which may recur 
several times, and which frequently lead to a fatal issue, we 
speak of eclampsia gravidarum or parturientium. If children, 
as not uncommonly occurs, have paroxysms, consisting of dis- 
tortions of the face, trismus-like clinching of the teeth, general 
spasms, and more or less marked disturbances of consciousness, 
we designate the affection as eclampsia infantum, and use the 
same term if at the onset or in the course of acute diseases or 
certain intoxications (more particularly lead poisoning) attacks 
occur characterized by (bilateral, more rarely unilateral) con- 
vulsions and loss of consciousness, which, therefore, differ clin- 
ically either not at all or only slightly from the genuine epilep- 
tic seizures. The nature of the attacks is as obscure as their 
aetiology. Whether in eclampsia parturientium the diminished 
excretion of urea has to be held responsible for the convulsions, 
and they thus are to be regarded as uremic, whether in the 
convulsions of children reflex action plays the chief role, or 
whether we have to deal with autointoxication in which dia- 
cetic acid occurs in the urine, is at least doubtful. Every one 
admits that, in the second form, dentition, digestive disturb- 
ances, or intestinal parasites play a certain part, yet there are 
certainly other factors which deserve consideration in this con- 
nection, for instance, heredity, a general neuropathic diathesis, 
the health of the parents, and the possible existence of rickets. 
The convulsions of children (eclampsia acuta infantilis) are 
extremely common. Clinically, all cases of this kind are very 
much alike, whereas serologically different cases differ greatly. 
In a given case we should, first of all, try to determine whether 
we have to deal with anatomical lesions (of the cortex, etc.), 
or whether these can be excluded ; and only by the most 
careful examination can we avoid errors and are we able 
to make a correct diagnosis. Cortical diseases (cerebral in- 
fantile paralysis), epilepsy, spinal paralysis of children, the 



ECLAMPSIA. 557 

initial stage of acute diseases, etc., must be taken into consid- 
eration. 

The prognosis is always doubtful, both in adults and in 
children, and the danger is usually greater in pregnant and 
parturient women than in children. Death not rarely occurs 
during the convulsions, as we have said above, and we may 
assume that out of a hundred cases of this kind there are thirty, 
forty, often fifty who die, and the danger increases with the 
duration of the labor and the long continuance of the pains. 
In children a fatal issue is often brought about by a spasm of 
the glottis, rarely by exhaustion. Recovery frequently is in- 
complete, and there may be left some psychical disturbances, 
amaurosis or disturbances of speech, etc. 

About the treatment of eclampsia the opinions are even at 
the present time very much divided. In pregnant or parturi- 
ent women cold affusions in a warm bath, as recommended by 
Scanzoni, also the application of large cantharidal plasters to 
the neck, ought to be resorted to as soon as possible ; from the 
nervines we can expect nothing. Mild laxatives, cautious 
venesection, regulation of the functions of diuresis and dia- 
phoresis are in most cases indicated. Often we have no time 
to think of such measures ; in urgent cases Veit (cf. lit.) has 
recommended large doses of morphine, beginning with three 
centigrammes (circ. gr. ss.) and increasing the dose to two or 
three decigrammes (grs. iij-grs. ivss.) a day. The eclampsia of 
children is, according to some, among them Henoch, best 
treated by inhalations of chloroform, which will soon stop the 
convulsions. One ought, they think, to first cut short the con- 
vulsions, and then proceed to find out their cause. Sometimes 
this advice is good, viz., in cases in which there exists no cere- 
bral lesion. If one does exist, or if there are grounds for sus- 
pecting it, the inhalation will prove to be of no use, and may 
rather have a bad effect. It will therefore be necessary to 
attempt to settle this question by as short an examination as 
possible. If we are unable to make up our minds, a tepid bath 
and cold affusions, vinegar enemata, or evaporating lotions, 
etc., to the skin can do no harm. For the beginning this suf- 
fices ; afterward it may be advisable to prescribe ice to the 
head in congestive conditions, possibly even leeches to the 
head, and in cases where collapse seems imminent, vinegar ene- 
mata, strong wine, or injections of ether. The nervines may 
as well be discarded in the treatment of the convulsions, as 



'553 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



they do no good in this stage ; they may, however, be used 
later when the immediate danger has passed. Wrapping the 
children in warm moist sheets (after the method of Priessnitz), 
while ice is kept to the head, I have known repeatedly to be 
effectual. On the whole, even these measures are not reliable, 
and the part which a physician plays in the presence of 
eclampsia of children is by no means enviable. 

LITERATURE. 

I. Epilepsy. 

a. Idiopathic Epilepsy. 

Albertoni. Arch. f. experiment. Pathol, und Pharmak., 1881, xv, 3, 4. 
Unverricht. Experimentelle und klinische Untersuch. iiber Epilepsie. Habili- 

tationsschrift, Breslau, 1883. (Contains all the older references.) 
Bourneville. Combarien et Seglas. Recherches clin. et therapeut. sur l'epilep- 

sie, l'hysterie, etc. Paris, 1886, vols. i-vi. 
Witkowski. Ueber epiieptisches Fieber und einige andere die Epilepsie betref- 

fende Fragen. Berliner klin. Wochenschr., 1886, Nos. 43, 44. 
Erlenmeyer. Die Principien der Epilepsiebehandlung. Wiesbaden, 1886. 
Homen. Beitrag zur Lehre von den epileptogenen Zonen. Centralblatt fur 

Nervenheilk., 1886, No. 6. 
Vdlkers. Centralbl. f. Nervenheilkunde, November 22, 1886. 
Jacquet. Annales de dermat. et syph., 1886, vii, 12. (On bromism.) 
Ozeretzkowsky. Ueber die Alteration der Sensibilitat bei Epileptischen. Med. 

Obosrenie, 1886, 9. 
Unverricht. Ueber experimentelle Epilepsie. Verhandl. des Congresses fur 

innere Med., Wiesbaden, 1887. 
Salm. Neurol. Centralbl, 1887, 11. 
Corning. New York Medical Journal, June 18, 1887. 

Leidesdorf. Wiener med. Wochenschr., 1887, 5, 6. (On epileptic equivalents.) 
Vetter. Deutsches Arch. f. klin. Med., 1887, Bd. xl, Heft 3, 4, 
Franck. Lecons sur les fonctions motrices du cerveau et l'epilepsie cerebrale. 

Paris: Doin, 1887. 
v. Bergmann. Die operative Behandlung der traumatischen Epilepsie. Deutsche 

militararztl. Ztg., 1887, xvi, 8. 
Bourneville et Bricon. De l'epilepsie procursive. Arch, de neurol., November, 

1888, xvi. 
Marie, P. Progr. med., 1888, xv, 43. 

Pepper. Phila. Medical and Surgical Reporter, November 25, 1888, Ivii. 
Jelgersma. Nederl. Weekbl., 1888, i, 1. (Pathogenesis.) 

Haig. Neurol. Centralbl, 1888, vii, 5. (Connection of epilepsy with the excre- 
tion of urea.) 
Binswanger. Arch. f. Psych, u. Nervenkrankh., 1888, xix, 3. (Experimental 

studies on the pathogenesis of the attack.) 
Fournier. Gaz. des hop., 1888, lxi, 105. (Epilepsy and syphilis.) 
Lemoine. Sur la pathogenie de l'epilepsie. Progr. med., 1888, 16. 



EPILEPSY. 



559 



Keen. Journal of the American Medical Association, 1888. 

Stevenson. Medical Press and Circular, 1888, 24, 10. 

Sighicelli. Riv. clin. e ter., June, 1888. 

Ladame. Ueber procursive Epilepsie. Internat. klin. Rundschau, 1889. 

v. Baracz. Wiener med. Wochenschr., 1889, 7, 8. (Ligation of the vertebral 
arteries.) 

Fere. Note sur l'etat des forces et sur le tremblement chez les 6pileptiques 
apres les attaques. Nouv. iconogr. de la Salpetr., 1889, ii, 1. 

Salzer. Ueber einen Fall von traumatischer Epilepsie. Wiener klin. Wochen- 
schr., 1889, ii, 5, 6. 

Wigresworth and Bickerton. On a Connection between Epilepsy and Errors of 
Ocular Refraction. Brain, 1889, xliv, p. 468. 

Wildermuth. Amylenhydrat gegen Epilepsie. Neurol. Centralbl., 1889, 15. 

b. Reflex Epilepsy. 

Boucheron. Deutsche Med. Zeitg., 1887, 97. ("Ear epilepsy.") 

Schloss. Wiener med. Wochenschr., 1888, xxxvii, 48. 

Dirmoser. Internat. klin. Rundschau, 1888, 33. (Fracture of the clavicle; at- 
tacks for three years ; recovery four months after operation.) 

Lloyd and Deaver. New York Medical Record, September 12, 1888, xxxiv. 
(Cure by trephining.) 

Boucheron. Revue mensuelle de laryng., etc., 1888, ix, 7. (" Ear epilepsy.") 

Nicolai. Deutsche Monatschr. f. Zahnheilk., 1889, vii, 1. (Epilepsy produced 
by difficult cutting of the wisdom tooth.) 

Brubaker. Journal of Nervous and Mental Diseases, February 2, 1888, xiii. 

Pins. Internat. klin. Rundschau, 1888, 20. 

c. Jacksonian Epilepsy. 

Unger. Wiener med. Blatter, 1886, xi, 40-44. (Jacksonian epilepsy in chil- 
dren.) 

Mendel. Ueber Jackson'sche Epilepsie und Psychose. Allgem. Zeitschr. f. 
Psych., 1887, 44, 2. 

Chauffard. De Puremie convulsive a forme de l'epilepsie jacksonienne. Arch, 
gener. de med., July, 1887, pp. 5 et seq. 

Bouchard. Les auto-intoxications dans les maladies. Paris, 1887. 

Lloyd. Boston Medical and Surgical Journal, October 15, 1888, cxix. (Cure by 
trephining and incising the motor region.) 

Lowenfeld. Ueber Jackson'sche Epilepsie. Miinchener med. Wochenschr., 
1888, xxxv, 48. 

Pitres. Revue de med., 1888, viii, 8. (Clinical equivalents of Jacksonian epi- 
lepsy.) 

Jackson, Hughlings. Brain, July, 1888, xi. 

Berbez. Gaz. des hop., 1888, 50. 

II. Eclampsia. 

Lewandowski. Berl. klin. Wochenschr., 1885, xxii, 37. 

Ballantyne. Sphygmographic Tracings in Puerperal Eclampsia. Edinb. Med. 
Journ., May, 1885, xxx, p. 1007. 



560 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



Proux. On the Treatment of Eclampsia Infantum. Bull, de therap., May 15, 

1885, cviii. (Recommends belladonna and chloral hydrate.) 
Rosenstein, L. Die Pathologie und Therapie der Nierenkrankheiten. Berlin, 

1886, 3. Aufl. 

Soltmann, O. Eclampsia infantum. Real-Encyclopadie der gesammten Heil- 

kunde. Wien und Leipzig, 1886. 
Virchovv, R. Ueber Fettembolie u. Eclampsie. Bed. klin. Wochenschr., 1886, 

xxiii, 30. 
Osthoff. Beitrage zur Lehre von der Eclampsie und Uramie. v. Volkmann's 

klin. Vortrage, 1886, 266. 
Stumpf. Miinchener med. Wochenschr., 1887, xxxiv, 35, 36. 
Pfannenstiel. Centralbl. f. Gynakol., 1887, xi, 38. (Death from apoplexy.) 
Baginsky. Archiv f. Kinderheilk., 1887, xi, 1. (Acetonuria in eclampsia.) 
Veit. Ueber die Behandlung der puerperalen Eclampsie. Volkmann's klin. 

Vortrage, 1887, No. 304. 
Hermann, Ernest. Transactions of the Obstetrical Society of London for the 

year 1887, vol. xxix, pp. 539-548. London, 1888. 
Lantos. Beitrage zur Lehre von der Eclampsie und Albuminuric Arch. f. 

Gynakol., 1888, xxxii, 3, p. 364. 
Feustell. Beitrage zur Pathologie und Therapie der puerperalen Eclampsie. 

Inaug. Diss. Berlin, 1888. 
Love. Weekly Medical Review, 1880, xix, 1. (Eel. infant.) 



CHAPTER IV. 

HYSTERO-EPILEPSY — MAJOR HYSTERIA — HYPNOTISM — TREATMENT BY 
SUGGESTION. 

The reason why we have not treated of the disease, we are 
about to describe, in immediate connection with hysteria, but 
have placed it after the chapter on epilepsy, is because the " at- 
tacks " of hystero-epilepsy appear to the observer as a result, 
or perhaps we had better say as a sort of mixture, of hysteria 
and epilepsy. It would, however, be a mistake to infer from 
this that the affection has any close physiological or patholog- 
ical connection with epilepsy. It is more likely that we ought 
to regard it as a higher, or indeed the highest, grade of hys- 
teria (cf. page 524). 

The " major attacks " have been studied exclusively by 
Charcot in the Salpetriere. To him alone and some of his 
pupils, more particularly P. Richer, we owe our knowledge of 
their nature and characteristics, and of the rules and definite 
laws which they appear to follow. Almost every, nay, we can 
well say every publication on hytero-epilepsy that did not 
emanate from the Salpetriere was, at any rate, based upon 
Charcot's observations and communications, and hardly any- 
thing new has come from any other source. 

The attacks can usually be divided into four distinct peri- 
ods, though one or other of them may so predominate, as re- 
gards its duration and intensity, that the rest are somewhat 
obscured. The first period embraces the epileptiform attacks : 
the body is suddenly shaken, respiration stops, the patient 
lets fall anything she happens to be holding in her hands, and 
is thrown to the ground. She is now seized with general 
convulsions or there develop rapidly extensive contractures 
affecting almost all the voluntary muscles. In the second stage, 
which immediately follows this, the patient is bounced up and 
down in bed, she assumes marvelous positions, stands on her 
36 



562 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

head, curves the body in the form of an arch {arc de cercle), 
and howls and roars at the same time like a wild beast. This 
is the period of major movements, " clownism." It is fol- 
lowed immediately by certain hallucinations, under the influ- 
ence of which the patients assume postures indicative of the 
most varied passions, the "attitudes passionelles" of the French. 
The face takes on, according to the particular hallucination, 
an expression of anger, rage, devotion, love, voluptuousness, 
curiosity, pain, etc., which would give us the impression that 
the patient is passing in her mind through a period of her life 
the details of which are unusually vivid in her memory. The 
postures and expressions may change, although sometimes 
they remain the same throughout this stage. That of the 
" crucified " has obtained a certain degree of celebrity, because 
it seems to be particularly frequent. Finally, the fourth stage 
is marked by a delirium, in which hallucinations recur with 
the greatest persistency, some patients imagining they see 
animals, others terror-inspiring objects of different kinds, and 
so forth. Automatic movements are not rare ; sometimes an- 
aesthesias or at least analgesias are noted. This delirium re- 
sembles in many respects an alcoholic intoxication. The dura- 
tion and frequency of the attacks vary greatly. Some only 
last from one to five minutes, and recur ten, twenty, or even 
one hundred times a day {/tat de mat). It is a characteristic 
feature, and one very valuable in the differential diagnosis, that 
firm pressure upon the ovaries invariably suffices to cut short 
an attack. 

If this pressure is exerted constantly, as can be done by means 
of belts provided with pads, the attacks may be kept off for quite a 
considerable time. At the celebrated ball which every year at mi- 
car erne is given to the hysterical and hystero-epileptic patients of 
the Salpetriere, in which, of course, only females take part, each 
dancer wears her belt. If this, owing to the movements in danc- 
ing, slips from its proper place, so that the pressure is taken off 
the ovaries even for a moment, a major attack comes on, and the 
patient, twisting and turning herself and presenting the most in- 
credible distortions, is removed from the ball-room, without causing 
the least interruption in the dancing. 

The outlook for complete recovery in major hysteria is not 
favorable. All attempts to cure the patients remain in many 
instances fruitless, as we may observe in the Salpetriere, where 



HYSTERO-EPILEPSY. 563 

some patients, in spite of the best care and the most excellent 
treatment, remain for years without presenting any marked or 
lasting improvement either with regard to the violence or the 
frequency of the attacks. 

Sometimes, especially if the patients come early enough 
under the care of the physician, immediate removal from their 
homes into an institution does much good. The attacks become 
rarer and cease entirely after a few months. The treatment in 
these institutions consists in the " feeding system," which we 
have mentioned on page 525, as well as the ice-cold douches, 
to which we have also alluded above. 

The brilliant success of Charcot in the treatment of hystero- 
epilepsy is due to these three factors: (1) The removal from 
home, (2) the cold douches, and (3) the feeding system. With 
the use of static electricity and the magnet, the results have 
been shown to be much less favorable, and we may consider 
that this procedure, as far as the treatment of the major at- 
tacks goes, has in the main been discarded (cf. the references 
to metallotherapy). 

Reliable and correct as are the descriptions given by the 
Charcot school of the major attacks, which we may incidental- 
ly remark are very rarely seen in Germany, accurately as we 
can follow up the different phases or periods of the attack in 
many such patients, we still must be very careful in accepting 
the accounts of the influence of hypnotism upon hystero-epi- 
leptics and the conditions produced thereby. 

In the Salpetriere the patients were hypnotized by means 
of fixation of the eyes, by the action of a bright light, or the 
sound of an instrument called a tam-tam, or by similar means ; 
and, as every one must know who has been present at Charcot's 
experiments, certain individuals were hypnotized in a very few 
seconds. According to Richer, who, as we said, has made the 
most careful studies of this subject in conjunction with Char- 
cot, which appeared in various numbers of the Arch, de neurol. 
from 1 88 1 to 1883, there may be distinguished four different 
stages : (1) The cataleptic, (2) the stage of suggestion, (3) the 
stage of lethargy, (4) the stage of somnambulism. 

In catalepsy, whether artificially produced or whether oc- 
curring spontaneously, as it does in hysteria in very exceptional 
cases, the members of the body remain in any position into 
which they have been put. Thus, if we passively bend the arm 
at the elbow and raise it up, it remains fixed in this position. 



564 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Flexion or extension in any joint can be produced without the 
slightest resistance on the part of the patient — " flexibilitas 
cerea " ; even the most unusual, uncomfortable, and strangest 
attitudes are retained without any difficulty. How this most 
remarkable regulation of the necessary innervation is brought 
about we do not know as yet, neither have we the slightest 
grounds whereupon to base any theory by which we could 
seek to explain this condition, which is not infrequently also 
associated with disturbances of consciousness. 

The state of hallucinations excited by slight stimulation of 
the special senses (in reality by suggestion), and designated as 
automatism, is characterized by total analgesia. The eyes re- 
main open, and it is a remarkable fact that positions which are 
given to the body evoke the corresponding expressions of the 
face, and, vice versa, the body assumes the corresponding posi- 
tion if on the face, by faradization of the muscles, a certain ex- 
pression — e. g., of sadness, hilarity, spite, voluptuousness, or 
fear — is produced. By firmly shutting the eyes of the patient 
it is claimed that the second stage may be converted into the 
third, the automatic into the stage of lethargy. In this latter 
the excitability of all the nerves and muscles is greatly in- 
creased, so that, for instance, slight pressure upon the stem of 
the facial suffices to bring about contractions in all the muscles 
supplied by that nerve. The contraction lasts much longer 
than the stimulation, and therefore takes on a tetanic character. 
At the same time the patient is apparently completely uncon- 
scious, and there is total anaesthesia. Now it is impossible to 
create hallucinations. The tendon reflexes are greatly exag- 
gerated. If we now stroke the patient lightly over the top of 
the head, the hyperexcitability vanishes and a new stage comes 
on, that of the hysterical somnambulism. In this condition the 
patient is susceptible to external influences, inasmuch as the 
organs of special sense are performing their functions to a cer- 
tain degree. He answers questions (with closed eyes and some- 
what automatically), carries out instructions, and so forth. By 
local stimulation of the skin — for instance, by vigorous rubbing 
— we are able to produce contractures. By energetic pres- 
sure upon the eyes the patient can again be transferred from 
the somnambulistic to the lethargic condition. The occurrence 
of hallucinations and illusions is not constant. 

For a long time the theory that this condition was peculiar 
to hysterical patients when hypnotized, just as the other condi- 



HYPNOTISM. 



565 



tions were peculiar to them when awake, was not doubted, and 
the so-called major hypnotism, as the hypnosis of the hystero- 
epileptics was called, created everywhere great astonishment 
and admiration, especially in those who could actually observe 
it in Charcot's clinic at the Salpetriere. It is only recently 
that doubts have been raised about the correctness of these 
claims of Charcot. Many are inclined to believe that the 
above-described four stages, which the hypnosis of hysteria 
presents, can be produced in any hypnotized individual and not 
only in those who are hysterical, and that therefore the " major 
hypnotism " is no neurosis at all and has no characteristics of its 
own. Whether the members of the Salpetriere school will be 
able to defend their former assertions, and what arguments 
they can put forth, and whether they will be able to continue 
to uphold the existence of different stages of hysterical hypno- 
sis after all possible sources of error have been excluded, we 
can not tell. How they will be able to demonstrate the neuro- 
muscular hyperexcitability as physiological and not perhaps as 
produced voluntarily, as many are inclined to think now, has to 
be left to the future to decide, and more especially to the abso- 
lutely necessary repetition of the experiments. Here it is our 
part only to show on what grounds Charcot's doctrines have 
been attacked, what proofs have been brought forward to show 
his doctrine to be untenable, and to state clearly the stand- 
point which is now generally held as regards the origin and 
the phenomena of hypnotism. 

This is not the place to enter into a consideration of the 
mysticisms and the charlatanisms of a man who a hundred 
years ago propounded the doctrine of the so-called magnetic 
fluid, which, emanating from the magnetizer, and being capable 
of spreading itself in space, could receive all impulses of mo- 
tion and impart them, but as a matter of historical interest and 
justice we are compelled to state that it was Franz Mesmer, 
born in 1733, who gave the first impulse to a movement which, 
founded on his arrogant and wild teachings, has passed through 
manifold phases, and to-day still exists, now that it has been 
found possible to sift the chaff from the wheat. Magnetism to- 
day has succumbed to the same fate as alchemy, and has been 
discarded, but both bore good fruit ; the one opened the door 
to chemistry, the other to hypnotic suggestion (Bernheim). 

The fact that there is no such thing as a magnetic fluid, that 
hypnosis and the phenomena occurring during it are entirely 



5 66 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

subjective in nature, and are to be attributed to external influ- 
ences upon the nervous system, was discovered by James 
Braid, of Manchester, in 1841, and we are justified in opposing 
" braidism " to " mesmerism " just as we oppose truth to false- 
hood. Braid concentrated the attention of those he wanted to 
put to sleep by making them keep their eyes fixed upon a 
bright object ; he assumed that the fatigue of the levator pal- 
pebral superioris, which was simultaneously produced, was the 
cause of a sleep during which the imagination was so active that 
spontaneous mental pictures, as well as impressions imparted by 
others, (" suggestions ") obtained the power of actual percep- 
tions. If such impressions are imparted frequently, according 
to his observation, a certain habit is established, so that it be- 
comes, cceteris paribus, easier and easier to put the patient to 
sleep. Braid was also acquainted with the fact that corre- 
sponding sensations and passions can be produced in hypno- 
tized persons by putting their facial muscles and their extremi- 
ties in appropriate positions, although he made no attempt to 
explain these phenomena physiologically. This has only been 
done quite recently, and even then the study was evoked only 
by a purely external stimulus, viz., the exhibitions which a 
Danish magnetizer named Hansen gave in the German cities. 
The impression which these made upon the public at large was 
of such an exciting and uncanny nature, and the whole thing 
was so puzzling to men of learning, that physiologists and neu- 
ropathologists were impelled to approach the subject to see 
whether the apparently supernatural and inexplicable could 
not be traced to natural physiological laws. One of the most 
prominent physiologists, Heidenhain, put forward the theory 
that, by weak but steady stimulation of the nerves of special 
sense, the cells of the cerebral cortex were induced to discon- 
tinue for a time their activity, thus causing the subcortical 
reflex centres to fall into a state of irritation, partly because, 
owing to this inactivity, the reflex inhibitory influence of the 
cortex was suspended, and partly because every impulse reach- 
ing the brain was propagated to a limited area which neces- 
sarily led to stronger excitation of the part of the excitomo- 
tor apparatus belonging to it. With this ingenious hypoth- 
esis, which many others — Weinhold, of Chemnitz, Griitzner, 
Rumpf, Berger, and Schneider among them — have accepted, 
we had to be satisfied, and for the physiologists the interest in 
the matter was thus exhausted, and the subject was abandoned. 



HYPNOTISM. 567 

In pathology and general practical medicine, including, as 
we shall see, surgery and obstetrics, the matter obtained a new 
and increased significance when, quite recently, the observa- 
tions, which twenty years ago had been made by an investiga- 
tor in Nancy, Liebeault, were again taken up. Liebeault had 
published a work in 1866 with the title Du sommeil et des 
etats analogues considerees surtout au point de vue de Taction 
du moral sur le physique, in which he expanded upon the ob- 
servations of Braid ; he showed that it only needed a concen- 
tration of the thoughts on a single idea, viz., the idea of going 
to sleep, to make the body immobile, and to produce a certain 
kind of sleep which, however, differs from the physiological 
form (suggestion theory of hypnotism). The same author was 
the first to show that neither an optical, an auditory, nor a tac- 
tile stimulus was necessary to bring about hypnosis, but that 
the impressions from outside, the suggestions that the sleep 
must and will occur, are perfectly sufficient ; the hypnotized 
sleeper— whose ideation, in contradistinction to that of the 
ordinary sleeper, remains in contact with that of the hypnotizer 
— can be influenced by the latter in his ideas and actions. The 
fundamental observations of Liebeault remained unappreciated 
for twenty years ; the work was not read, hypnotism remained 
a curiosity, and it seemed inadvisable for a scientific physician 
to occupy himself with it, unless he was willing to gain for 
himself the reputation of a charlatan or of a man whose actions 
were suspicious or even dangerous. The credit of bringing to 
light the work of Liebeault, we might almost say of having 
discovered Liebeault, belongs to Bernheim, of Nancy, whose 
merit was still more augmented by his own contributions to 
the subject. He published his first article on hypnotism in 
1884, and with his book, De la suggestion et de ses applica- 
tions a la therapeutique, he has, to use a popular but express- 
ive phrase, "hit the nail on the head." He and the Nancy 
school have to be regarded as the founders of the successful 
attempt to make a systematic use of hypnotism for thera- 
peutic purposes, and when once the treatment by suggestion 
becomes generally accepted, and becomes an integral part of 
our therapeutic armamentarium, although at present there 
seems little prospect of this, Bernheim will be mentioned as 
its scientific originator. The adverse attitude which certain 
well-known scholars and investigators have thought proper to 
adopt toward the treatment by suggestion, we can well under- 



568 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



stand, if we remember that for the practice of hypnotism much 
time and patience is needed which is not at the disposal of 
everybody, but this opposition can do no permanent harm to 
the method if it is really good, since men like Krafft-Ebing 
and Forel, with their names as scientific investigators, and emi- 
nent practitioners like Wetterstrand, in Stockholm, and van 
Renterghem, of Amsterdam, and others, with their reputa- 
tion as physicians, have ranged themselves on the other side. 
The attempt also, which has been made from various quarters, 
to be done with the whole matter and stifle it by pronounc- 
ing it, in a lordly manner, a humbug, must be considered 
to have utterly failed, and the second argument of the oppo- 
nents, now put most prominently forward, that the use of hyp- 
notism in therapeutics is dangerous, and should be prohibited 
by law, will be groundless and without effect if hypnotism is 
never used carelessly and promiscuously, and if, what is very 
important, it remains in the hands of those whose calling it is 
to make use of therapeutic measures — that is, in those of the 
physicians. Nobody, certainly, who is acquainted with hyp- 
notism will deny that pathological conditions may be produced 
by it and that it may be dangerous, but is this a ground upon 
which to simply discard it without a further hearing ? Have 
we given up chloroform narcosis because it has now and then 
proved dangerous in the hands of the inexperienced and care- 
less operator, or have we given up the use of morphine on 
account of its poisonous action when used too freely and for 
too long a period of time? As in all other measures, we must 
recognize here indications and contraindications, and this can 
be done in the majority of cases without difficulty ; and as 
everything in this world, especially in the practice of medi- 
cine, even the smallest operation — that of vaccination, for ex- 
ample—has to be learned, so the art of hypnotizing has to be 
acquired, and one can expect to comprehend the subject and 
to have success with the practice of the treatment by sugges- 
tion only after careful and painstaking study. 

The technique of hypnotizing is somewhat as follows : The 
patient, having been placed in a comfortable armchair, is asked 
to think of nothing else than of going to sleep. We " suggest " 
to him that he is beginning to feel tired, that he is no longer 
able to completely open his eyes, which are already beginning 
to close, etc. At the same time he is asked to look steadily at 
two fingers of the hypnotizer, which at first are held directly 



HYPNOTISM. 



569 



in front of his eyes, but are gradually lowered, by which pro- 
cedure the closing of the eyes, which we desire, is easily accom- 
plished. Now either a difficulty in moving the arms or legs 
is suggested, a loss of sensation in certain parts of the skin, or 
some similar idea. The tone of voice in which all this is said 
should not be loud, but monotonous. The same suggestions 
must again and again be repeated, and care must be taken that 
disturbing noises, the slamming of doors or the striking of 
clocks, and such like, be not heard, so that the mind of the 
patient may as much as possible be concentrated upon the hyp- 
notizer. Sometimes, but by no means always, the very first 
attempt to bring about hypnosis is successful, as I have seen 
in some of Forel's as well as Wetterstrand's cases, and the hyp- 
nosis may be so profound that we can already venture to give 
therapeutic suggestions. Sometimes the first, second, and 
third attempts fail completely or partially ; then we must, if no 
contraindications exist, try again and again, but under no con- 
sideration should the individual trials be prolonged beyond 
two or three minutes. Without question external circum- 
stances are of great significance. If a patient who is to be hyp- 
notized enters a room, in which eight, ten, or twelve persons 
are lying sound asleep stretched out on easy-chairs and sofas, 
and is left sitting there quietly for a quarter of an hour with- 
out any attempt to put him to sleep, his suggestibility — that is, 
his susceptibility — will sometimes be materially increased, and 
it will be a comparatively easy matter to hypnotize him. But 
there are certain internal conditions also which may throw 
great obstacles in our way, and which must, therefore, not be 
overlooked. Thus, if a patient does not believe that he can be 
put to sleep, or if he makes up his mind to resist us, a certain 
amount of finesse is necessary ; we have to outwit him in order 
to produce hypnosis without his consent or even against his 
will. Such exceptions, and the behavior of the physician who 
has to contend with them, can not here be treated of. Only 
one artifice we may mention which we have repeatedly used 
with very good results in producing hypnosis quickly and 
surely. We apply a large curved sponge electrode (anode) to 
the forehead, a second to the neck, close the circuit and allow 
a very weak (constant) current, just sufficient to produce the 
characteristic taste upon the tongue, to pass through the head 
for a few seconds, and then, without the knowledge of the pa- 
tient, open the circuit and tell him that the electricity passing 



through the brain will put him to sleep, and as a matter of fact 
this " suggested " current does so very promptly and surely. 
Secondly, the mental condition of the patient may stand in our 
way. It is an observation confirmed by all investigators that 
it is difficult or impossible to hypnotize insane patients, and 
that hysterical patients and hystero-epileptics are the least fa- 
vorable subjects. In the domain of psychiatry the treatment by 
suggestion, so far as we can judge at present, remains without 
significance ; on the other hand, it seems as if certain disturb- 
ances in nutrition — for example, general anaemia and chlorosis 
— facilitate hypnotization greatly, while an absolute confidence 
in the physician, the absence of all attempts to analyze and to 
test our procedures on the part of the patient while we are 
trying to hypnotize him, will also materially increase the sus- 
ceptibility to suggestions. If all factors, favorable and unfa- 
vorable, are taken together, we may say that by far the greater 
number of people can be hypnotized ; perhaps one might go so 
far as to say all, without exception, are susceptible if time and 
circumstances allow sufficient repetitions of the trial. For hos- 
pital practice the dictum of Bernheim may for the present be 
accepted, that the physician who does not succeed in hypno- 
tizing eighty per cent of his patients for therapeutic purposes 
does not understand the method. 

The manner in which hypnosis comes on and the phenomena 
observed during this state are extremely varied. Sometimes 
the eyes close suddenly and the patient is asleep at once ; 
more frequently this is preceded by twitchings of the lids, and 
moisture in the eyes, which are repeatedly closed and opened. 
Sometimes the lids are shut during hypnosis, sometimes a fine 
tremor is noticeable in them ; again, fibrillary twitchings in the 
muscles of the face may be remarked. The hypnotic influence 
does not always produce sleep, but there are different degrees, 
from the waking state to slight dullness of the senses and som- 
nolence, and, finally, deep sleep, which latter is called somnam- 
bulism. Bernheim in his explanation bases his arguments upon 
the ideas of Luys, that the different layers of the cortex are en- 
dowed with different functions : those nearest the surface are 
supposed to serve for the sensorium, the middle ones for the 
mental faculties, and the deepest for the transference of the 
will. He distinguishes accordingly nine degrees of hypnosis, 
and characterizes them in the following manner: (i) The pa- 
tient remains quiet with closed eyes during the suggestion, but 



HYPNOTISM. 



571 



can open them without difficulty when asked to do so, and 
claims not to have slept at all. (2) The patient is not able to 
open his eyes when asked. (3) The patient presents suggested 
catalepsy and analgesia, and remains in the position in which 
he is placed, but is able, after it has been suggested to him, 
to change from one position to another without assistance. 
(4) The patient is no longer able by himself to overcome 
the suggested catalepsy, and automatic, rotatory movements, 
especially of the arms, can be evoked. (5) Besides the catalepsy, 
contractures can be produced which the patient himself is not 
able to do away with. (6) The patient presents an automatic 
obedience ; he stands motionless if ordered to do so, he rises, 
walks, and acts, in fact, just as the hypnotizer may suggest. 
Intelligence and the activity of the senses are intact in these 
six stages. The patient on awakening remembers everything 
that has been done to him. (7) In the seventh stage the patient 
presents the same phenomena as in the preceding six stages, 
but on awakening has quite forgotten what has been going on. 
(8) Besides this amnesia on coming to, hallucinations can be 
produced during hypnosis which vanish after the return to the 
normal condition. (9) The suggested hallucinations persist 
after waking up — post-hypnotic suggestions — everything that 
can be produced in a patient when in a state of hypnosis can 
be brought about after he has awakened simply by suggesting 
to him during hypnosis that it will happen after he has awak- 
ened. In this possibility, of exerting an influence upon the pa- 
tient for a longer or shorter time after he is awake, lies the whole 
therapeutic significance of the treatment by suggestion. This 
(post-hypnotic) action, which in certain cases can be obtained in 
no other way than by suggestion, is sufficiently important to 
warrant and insure to hypnotism a lasting place in science. It 
is unnecessary to distinguish nine different stages of hypnosis 
as Bernheim did ; three are quite sufficient (Forel). The first 
is the stage of somnolence, corresponding to Bernheim's first 
stage ; the second is that of hypotaxia (light sleep), embracing 
all the stages from the second to the sixth of Bernheim ; the 
third is the stage of deep sleep (somnambulism), corresponding 
to the seventh, eighth, and ninth of Bernheim's classification. 
It is of practical importance to note that frequent hypnotizing 
usually increases the susceptibility of the patient, and that we 
can only succeed after repeated successful trials in producing 
deep sleep with amnesia, and be able to expect that our post- 



5/2 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



hypnotic suggestions will be carried out. This is the rule, al- 
though we occasionally meet with individuals in whom on the 
first trial we are able to recognize all the characteristics of the 
state of somnambulism. 

What are, then, the diseases in which we can, with good 
conscience and good hopes of success, venture to employ the 
treatment by suggestion ? We need hardly say that affections 
in which we have to deal with inflammatory processes, new 
growths, infections, or, in a word, with organic lesions, do not 
belong to this class ; and, as a matter of fact, it would hardly en- 
ter any one's head to attempt to cure pneumonia, typhoid 
fever, brain tumors, syphilis, tetanus, etc., by means of hypno- 
tism. It is a different matter if we are dealing merely with cer- 
tain symptoms of such maladies, for instance, insomnia, diffi- 
culty in breathing, or pains of the most varied kinds, not exclud- 
ing the lancinating pains of tabes. Here hypnotism should, at 
least, be given a trial, yet the main field in which the treatment 
by suggestion should be employed will not be the diseases we 
have mentioned, but rather all those which we have designated 
and described as functional disorders of the nervous system. 
Here, motor as well as sensory disturbances can be influenced, 
various neuralgias, including tic douloureux and migraine-like 
paroxysmal headache, sensory paralyses, the anaesthesias and 
parsesthesias of hysteria, etc., symptoms of motor irritation and 
paralysis, tic convulsif, writer's cramp, chorea, the tremor of 
paralysis agitans, and so forth. According to Forel, it is pos- 
sible to influence certain somatic functions to some extent — 
e. g., the menstruation and digestion— in such a manner that the 
menses can be brought on at a certain day and a certain hour, 
and a regular evacuation of the bowels every day can be in- 
sured by suggestion. Although these accounts come from the 
most indubitable source, the experiments must again be tested 
and confirmed. They can certainly only be successful, we 
should think, in individuals who have repeatedly been hypno- 
tized and are, as it were, " trained." With the treatment of 
alcoholism by suggestion Forel has had uncommonly good re- 
sults in his institution. The heaviest drinkers were not only 
for a time, but lastingly cured ; but no little influence certainly 
has here to be attributed to the temperance societies, which 
such individuals entered. Without constant watching and 
moral support, relapses would surely occur in such patients ; 
nevertheless, the influence of hypnotism in inebriety is of 



HYPNOTISM. 



573 



great importance. The behavior of morphinists toward sug- 
gestion has yet to be studied. The results so far obtained 
seem not to be very encouraging. The communication of 
Wetterstrand (cf. lit.) that it is possible in idiopathic epilepsy to 
diminish the frequency and severity of the attacks deserves to 
be remembered and tried in cases in which bromides are not 
well borne. Finally, we would call attention to the anaesthesia 
and analgesia which can easily be produced by suggestion, and 
which in surgery, as well as in obstetrics, may be very useful. 
I was present at Forel's clinic at the extraction of two obstinate 
teeth, which, after the proper hypnotization, were taken out 
without the slightest sign of pain on the part of the patient. 
Possibly the pains during labor may be removed by hypno- 
tism. The anaesthesia of the mucous membrane of the fauces 
may be very valuable in making laryngoscopical examinations 
and the like. We purposely refrain from entering into further 
details, but shall content ourselves with advising every one, 
who approaches the subject of treatment by suggestion with 
sufficient true and serious interest, to study the work of Bern- 
heim, which constitutes the foundation of this subject. 

LITERATURE. 
I. Hypnotism — Treatment by Suggestion (from the Year 1887). 

a. General. 

All the older references have been collected by Mobius (cf. Schmidt's Jahrbucher, 1881, Bd. 

190, P- 73)- 
Berillon. La suggestion et ses applications a la pedagogie. Gaz. des hop., 

1887, 123. 

Binswanger. Deutsche med. Wochenschrift, 1887, xiii, 42. (Present state of 

hypnotism.) 
Fontan et Segard. Elements de medecine suggestive. Paris, O. Doin, 1887. 
Bernheim. De la suggestion et de ses applications a la therapeutique. Paris. 

1888, second edition. 

Baierlacher. Munchner med. Wochenschrift, 1888, xxxv, 30. 

Krafft-Ebing. Eine experimentelle Studie auf dem Gebiete des Hypnotismus. 
Stuttgart, 1888.— English translation by Charles G. Chaddock. G. P. Put- 
nam's Sons. The Knickerbocker Press, 1889. 

Lagrave, C. de. Hypnotism. Paris, 1888. 

Maack. Zur Einfiihrung in das Studium des Hypnotismus und thierischen Mag- 
netismus. Berlin und Neuwied, 1888. 

Meynert. Wiener klin. Wochenschr. Wien, 1888, i, 22, 24. 

Schrenck-Notzing, v. Ein Beitrag zur therapeutischen Verwerthung des Hyp- 
notismus. Leipzig, Vogel, 1888. 



574 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



Seeligmiiller. Der moderne Hypnotismus. Deutsche med. Wochenschr., 1888, 

xiv, 31-34. 
Sallis. Ueber hypnot. Suggestionen, deren Wesen, klinische und strafrechtliche 

Bedeutung. Neuwied, 1888. 
Corey. Boston Med. and Surg. Journ., November 20, 1888, lxix. (Therapeutic 

value of hypnotism.) 
Feldmann. Berl. klin. Wochenschr., 1888, xxv, 44. 
Forel. Schweiz. Corresp.-BL, 1888, xviii, 23. (The value of hypnotism for the 

general practitioner.) 
Herter. Boston Med. and Surg. Journ., November 20, 1888, cxix. 
Mason. Ibid., November, 1888. 
Bernheim. Hypnose durch Suggestion. Wien. med. Presse, Wien. med. 

Wochenschr., 1888, xxviii, 26. 
Jendrassik. Neurol. Centralbl., 1888, 10, 11. 

Meynert. Ueber Hypnotismus. Wien. med. Presse, 1888, xxix, 24. 
Weiss, D. Prager med. Wochenschr., 1888, xiii, 20, 21. 
Wetterstrand. Om hypnoptismens anvandande i den praktiska medicinen. 

Stockholm, Seligmans, 1888, 3 Uppl. 
Freud. Wien. med. Bl., 1888, xi, 38, 39. 

v. Krafft-Ebing. Ueber Hypnotismus. Deutsche med. Ztg., 1888, 16, p. 196. 
Dessoir. Bibliographic des modernen Hypnotismus. Berlin, 1888. 
Binswanger. Therapeut. Monatshefte, 1889, iii, 1, p. 1. 
Moll. Archiv f. Psych., 1889, xx, 2. 
Moll. Der Hypnotismus. Berlin, 1889. 

Liebeault. Du sommeil provoque. Second edition, Paris, 1889. 
Forel. Der Hypnotismus, seine Bedeutung und seine Handhabung. Stuttgart, 

Enke, 1889. 
Liegeois. De la suggestion et du somnambulisme dans leurs rapports avec la 

jurisprudence et la medecine legale. Paris, Doin, 1889. 
Baierlacher. Die Suggestivtherapie und ihre Technik. Stuttgart, 1889. 
Beaunis. Le somnambulisme provoce. Etudes physiologiques et psychologiques. 

i2e, Paris, 1886. 

b. Special ( Various Cases cured or treated by Hypnotic Suggestion). 

Sollier. Progr. med., 1887, 42. (Hystero-epileptic attacks said to have been 
cured.) 

Mialet. Gaz. des hop., 1887, 116. (Hyperemesis gravidarum cured.) 

Obersteiner. Klinische Zeit- und Streitfragen. Wien, 1887, No. 2. 

Birdsall. Boston Med. and Surg. Journ., November 20, 1888, cxix. (Tremor.) 

Frey. Wien. med. Presse, cxix, 50, 51. (Neuralgia of the fifth cured.) 

Frey. Ibid., xxix, 25. (Sleeplessness cured.) 

Baierlacher. Miinchener med. Wochenschr., 1888, xxxv, 39. (Report of 
cases.) 

Konigshofer. Klin. Mon.-Bl. fur Augenheilkunde. Januar 1888, xxvi. (Func- 
tional eye trouble.) 

Hackel. Die Rolle der Suggestion bei gewissen Erscheinungen der Hysterie 
und des Hypnotismus. Jena, 1888. 

Forel. Schweiz. Correspond.-Bl., 1888, xviii, 6. 

Nonne. Neurol. Centralbl., 1888, vii, 7, 8. 



HYPNOTISM. 



575 



Ribot. Revue med. de la Suisse Rom., March, 1888, viii, 3. (Hysterical hemi- 
plegia cured.) 

Treulich. Prag. med. Wochenschr., 1888, xiii, 12. 

Scheinmann. Deutsche med. Wochenschr., 1889, 21. (Hysterical aphonia 
cured.) 

Michael. Deutsche med. Ztg., 1889. 63. (Epilepsy improved for a time, hys- 
tero-epilepsy and hysterical aphonia cured.) 

2. Metallotherapy. 

Burq. Gaz. des hop., 1878, 91, 96, 102, 105, 106. 

Charcot. Gaz. des hop., 1878, 87, 135. 

Debove. L'Union, 1879, 54. 

Dumontpallier. La metallotherapie ou le Burquisme. Paris, 1880. 

Vigouroux. Metallotherapie, metalloscopie, assthesiogenes. Paris, 1882. 

Babinski. Prog, med., 1886, xiv, 47. 



PART II. 

DISEASES OF THE GENERAL NERVOUS SYSTEM 
WITH KNOWN ANATOMICAL BASIS. 

The anatomical changes, which are found in the diseases 
belonging to this category, concern the central nervous system 
as well as the peripheral nerves. The former always suffers, 
the latter are only in certain cases affected. Whether the 
changes in the peripheral nerves are to be regarded as second- 
ary, or whether the entire nervous system becomes affected in 
all its parts at the same time, so that the peripheral and the 
central lesions progress pari passu, can not be definitely de- 
cided. The nature of the anatomical changes will be discussed 
under the head of each individual affection. 



CHAPTER I. 

MULTIPLE SCLEROSIS — DISSEMINATED SCLEROSIS — INSULAR SCLE- 
ROSIS — SCLEROSE EN PLAQUES — SCLEROSIS CEREBRO- 
SPINALIS DISSEMINATA S. MULTIPLEX. 

Although multiple sclerosis is not one of the common 
affections of the nervous system, it is desirable and important 
for the general practitioner to possess a clear understanding 
of it, because the clinical appearances by which the different 
cases manifest themselves vary within such wide limits and 
remind us now of this, now of that spinal or cerebral affection, 
without ever completely simulating any one definite disease. 
The typical course given in the books is not very often met 
with in practice. Much more commonly one or the other of 
the classical symptoms is not present at all, or, if present, only 
very slightly developed. On the other hand, symptoms are 
occasionally encountered which are not included in the usual 



MULTIPLE SCLEROSIS. 



$77 



descriptions of the disease. In a word, multiple sclerosis is 
very inconstant in its manifestations, a circumstance which 
often makes the diagnosis very difficult. In the investigation 
into the pathology as well as the clinical aspect, Charcot has 
done admirable and lasting service. 

Symptoms and Course. — The course of a classical case is 
usually as follows : The patient first complains of general 
symptoms — headache, vertigo, digestive disorders — soon, also, 
of sensory disturbances in the upper and lower extremities, 
slight weakness, and a readiness to become fatigued. These 
symptoms may persist for months, yet relatively early one or 
several apoplectiform attacks may occur which sufficiently in- 




tlJH^.AJfi" 



-*ku if*...'S*>* 



&L,£ 









Fig. 161.— Specimen of Handwriting in a Case of Multiple Sclerosis. (Ich hefce 
(heisse) Henriette Sterner, bin 48 Iahre alt. Breslau, den 19 Juni). 

dicate the seriousness of the condition. It strikes the patient, 
as well as those who surround him, as a peculiar thing, that 
whenever he attempts to pick up something with his hands, or 
to make any other movement, a tremor appears which frus- 
trates the intended movement more or less completely. If he 
attempts to raise a full glass to his mouth, he spills some of the 
contents. If he attempts to eat, the food is jerked off his fork, 
etc. Co-ordinated movements, such as are required for writing 
or playing the piano, become difficult, the handwriting becomes 
almost illegible (Fig. 161), and the condition is materially ag- 
gravated if the tremor is not confined to the upper, but if also 
the lower extremities, the trunk, neck, and head are attacked, 
so that on voluntary movements — on attempts to walk, for in- 
stance — the whole body first begins to tremble, and finally 
37 



578 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



shakes so violently that the patient is forced to sit or lie down 
at once. This symptom, which is almost pathognomonic for 
multiple sclerosis, or at any rate most significant, is called "in- 
tention tremor," a term which does not, however, implv that 
the tremor is "intentional," but only that it appears on volun- 
tary (" intended ") movements. During rest no trace of it is 
observed. When the patient lies quietly and undisturbed in bed 
no tremor is present, whereas, if he is spoken to, examined, 
made to answer questions, and the like, a tremor over the 
whole body develops, which of course presents various degrees 
of intensity. It is most marked and characteristic if the patient 
is asked to bring his hand slowly to an object — for instance, to 
a pin laid upon the table. At first the motion is fairly good 
and steady, he trembles but little or not at all, but the closer 
he approaches to the pin the more unsteady becomes the hand 
and the larger become the excursions of the tremor, so that to 
grasp the pin becomes impossible. In some exceptional cases 
I have seen the shaking movements appear on one side only, 
so that the patient was capable of performing normal move- 
ments with one hand and one leg, when those of the other 
side had become entirely useless. 

In this intention tremor the eye muscles also take part ; 
as soon as the patient attempts to fix a point with his eyes 
nystagmus appears, which, however, differs from the tremor 
of the other voluntary muscles, inasmuch as it does not com- 
pletely disappear during rest. As a subjective symptom the 
very annoying sensation of giddiness must be mentioned in 
this connection, which leaves the patient only when he lies 
quietly in bed, whereas it otherwise impedes him a good deal 
in his movements, especially in walking. Owing to the faulty 
innervation of the tongue and larynx, we meet with a peculiar 
speech disturbance ; the patient talks slowly, in a monotonous 
tone, and awkwardly, and his speech is scanning, as he makes 
a pause after each word, almost after each syllable, so that it 
takes him a much longer time to express his thoughts than a 
healthy man : " Yes — doctor — I — am — very — much — fa — tigued 
— and — worn — out." As this is spoken in the manner indicated, 
without any change of intonation it is very characteristic in- 
deed, and it is, together with the intention tremor and the 
nystagmus, pathognomonic for multiple sclerosis. It impresses 
itself so much upon the mind that once heard it can never be 
forgotten or misinterpreted. 



MULTIPLE SCLEROSIS. 



579 



To give a physiological explanation of the intention tremor 
is out of our power, and it is more especially not clear why 
it is so extremely common in multiple sclerosis, where we have 
such an irregular distribution of the anatomical lesions, where- 
as in most of the other cerebral affections it is absent. Whether 
Charcot's idea is correct, according to which the long persist- 
ence of the axis cylinders in the sclerotic foci has some connec- 
tion with the tremor, or whether we should hold with Strum- 
pell that the loss of the myeline sheaths, in consequence of 
which an abnormal diffusion of the nerve current from fibre to 
fibre occurs, is responsible for this, we can not decide, nor have 
we any proof of the correctness of Stephan's view (cf. lit.) that 
the existence of sclerotic foci in the thalamus gives rise to the 
phenomenon, nor of Cramer's (cf. lit.) that the intention tremor 
has to be explained as analogous to the tremor which comes 
on after hard muscular exertion. 

Though we may be justified in looking upon these three 
symptoms as constituting in a manner the typical picture of 
multiple sclerosis, we must, as we have said above, at once 
familiarize ourselves with the fact, that even these may not all 
be pronounced, or again that there may be others to be found 
in conjunction with them, developing in the course of the dis- 
ease. Among these latter we may mention certain spastic 
symptoms, rigidity of the muscles, increased tendon and skin 
reflexes, the above-described spastic walk — which, together, are 
liable to simulate, at least for a time, the picture of spastic spinal 
paralysis. This is the more likely as there are no sensory dis- 
turbances at all to be noted in multiple sclerosis; only in rare 
exceptions paraesthesias are observed, owing to which tabes 
and myelitis may be diagnosticated, especially if, as sometimes 
happens, bladder disorders are superadded. That these latter 
are by no means as rare in multiple sclerosis as was formerly 
supposed, has recently been pointed out by Erb, and after him 
by Oppenheim (Deutsche med. Ztg., 1889, 32). Glycosuria 
will be found associated with the disease if there are foci sit- 
uated in the floor of the fourth ventricle (Richardiere, Revue 
de med., July, 1887). 

Participation of the optic and other cranial nerves is not 
very rare, yet it is here much less important for the diagnosis, 
and much less significant for the course of the disease than, for 
example, in tabes. Diplopia is rarely met with ; and equally 
uncommon is the neuritis and atrophy of the optic which leads 



58o 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



to amaurosis. Uhthoff (cf. lit.) has recently pointed out in an 
admirable study, that if optic atrophy occurs it is not like the 
primary atrophy in tabes, but that here it is a secondary pro- 
cess, which follows an active increase of the fine connective- 
tissue elements. It is self-evident that various disorders of 
sight are associated with this, yet they often present tem- 
porary improvement, and have usually a less serious issue than 
those of tabes. In general, it is characteristic of multiple scle- 
rosis that its course is not uninterruptedly progressive, but that 
it shows remissions, during which the hopes of the patient as 
well as of his friends for his complete recovery are aroused. 
1 have seen instances in which such remissions lasted for years 
and the symptoms disappeared to a great extent, and in which, 
just owing to this peculiarity in the course of the disease, the 
diagnosis could be made with some certainty. 

Cerebral manifestations are not uncommon, and frequently 
a slight degree of dementia — a psychical weakness — develops, 
which to the patient himself makes his condition more bear- 
able. It must also be regarded as a sign of beginning mental 
weakness, I think, that in some cases the patient frequently 
laughs boisterously without a cause. One of my patients had 
spells of loud laughter, which lasted from one to three minutes, 
and which appeared usually without sufficient motive. I have 
never had occasion to observe pronounced states of depression 
or exaltation in the course of this disease. The vertigo, which 
of course must also be regarded as a cerebral symptom, has 
been spoken of above. Apoplectiform attacks in the beginning 
of the disease are not rare ; epileptiform seizures may be found, 
if the cerebral cortex is more especially implicated. 

It has been shown by Charcot that in certain cases the 
development of the symptoms appears to be abortive and the 
affection, one might almost say, remains latent and can only be 
recognized by the peculiar shaking tremor. He proposed for 
these instances Trousseau's designation, " formes fnistes" and 
it seems that in multiple sclerosis such forms are observed 
relatively frequently. As an example of the general course 
which the disease may run I insert here the following history 
of a patient in my wards, who is still living : 

Paul W., thirty-one years old, began to be sick ten years ago, 
during his military service. At first, at times he could not feel his 
rifle in his left arm, and then in the same year he was often conscious 



MULTIPLE SCLEROSIS. 58 1 

of a slight feeling of fatigue, which was associated with vertigo. He 
had a good deal of difficulty with his arms and his legs ; they always 
felt as if they were asleep, and any muscular action necessitated 
the greatest exertion. He could not go through his salutes in the 
proper manner, and he was repeatedly punished on this account. 
At the same time he had now and then vomiting and weakness of 
the bladder for quite a long time, so that, on coughing, small quan- 
tities of urine were passed involuntarily. On examination, we are 
told, Romberg's sign was absent and the patellar reflexes were in- 
creased. A few months later, marked weakness in the right arm and 
the right leg became manifest, and the acuteness of hearing became 
diminished on that side. The patient complained of an annoying 
double vision. In 1879 he had some difficulty in swallowing; the 
bolus would stick in his throat, so that he had to force it down. In 
1880 pronounced deliberation in speaking is said to have been notice- 
able, and the patient at that time also complained that he could not lay 
his tongue upon certain words which he wished to use. The speech 
disturbance soon passed off, but the patient suffered from various 
troubles till January, 1884, in which month I saw him for the first 
time. He then presented the symptoms of an incipient tabes, but it 
was noted as a remarkable feature that the patellar, reflexes were 
retained. The lancinating pains, however, the paresis of the legs, 
the diplopia, the paresis of the bladder, the unsteadiness, which ap- 
peared especially in the dark, seemed sufficient to warrant the diag- 
nosis of tabes, and, in the out-patient department, this diagnosis was 
made, although with some reservation. The patient declined to 
enter the hospital. He was therefore ordered galvanism, but was 
lost sight of in the summer of 1884. Two years later he was treated 
at a hospital in this city for six months. Although I was unable to 
obtain a record of the case, I heard that the tabetic symptoms were 
very indistinct, and that the condition suggested rather a spastic 
paralysis. The patient was again lost sight of. Finally, on Janu- 
ary 8, 1888, he was admitted to the medical ward of the city alms- 
house, where he still remains. From a note made on January 10, 
1888, the following is extracted : The patient is a well-nourished 
man ; as he lies quietly in bed, the general aspect suggests nothing- 
abnormal ; if, however, he is asked to perform any movement, the 
whole body — trunk, head, and extremities— are seized with a violent 
shaking tremor, which makes it difficult for him to get up, and im- 
possible for him to walk without assistance from another person, 
even when supported by two canes. If he is allowed to discontinue 
all attempts at moving, the tremor gradually abates, and five or ten 
minutes later he is perfectly quiet again. The patient is unable to 
feed himself, and can not occupy himself with anything. The raus- 



582 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

cular strength is retained everywhere. In the domain of the cranial 
nerves nothing but nystagmus can be noticed, which is especially 
well marked on the right side. The facial, hypoglossal, etc., are 
normal. The tongue is protruded steadily and straight. Speech is 
slow, although not distinctly scanning. There are no motor or sen- 
sory speech disturbances. The tendon reflexes in the upper, but 
more especially in the lower extremities, are increased, and the skin 
reflexes are without exception well marked. Sensory changes can 
nowhere be demonstrated, and the bladder disturbances, which were 
present on previous occasions, have disappeared. The spinal column 
is nowhere tender on pressure. Among the subjective complaints 
of the patient the dizziness is alone to be mentioned, which, however, 
even if the shaking movements were not present, in itself would be 
sufficient to keep him from doing anything. 

As a result of this examination the diagnosis of multiple sclerosis 
was made, and will certainly be proved to be correct at the post- 
mortem examination. It is interesting, however, that in this case 
the course of the disease suggested in its initial stages Thomsen's 
disease (although not congenital), later tabes (with retained knee- 
kick), then spastic spinal paralysis (conjectural diagnosis), before 
the picture of insular sclerosis developed. 

Diagnosis. — The diagnosis presents difficulties in almost 
every case, owing to the protracted course and the changes in 
the picture of the disease during the different periods. Even 
the most careful examination will not always keep us from 
errors, and we must never be surprised if the autopsy does not 
always confirm the diagnosis made during life. The case of 
Westphal in which a multiple sclerosis was diagnosticated, 
but where post mortem no lesions at all were found, has been 
alluded to before. In another instance, reported by Frey (cf. 
lit), there was found, instead of the confidently expected foci 
of sclerosis, a leptomeningitis, and similar errors would not be 
difficult to find on a careful perusal of the literature. The pos- 
sibility that we are dealing with hysteria, in a given case, must 
always be considered, and then, of course, great weight must 
be laid upon the presence of other symptoms which would 
indicate such a condition. 

Pathological Anatomy. — The anatomical changes of multi- 
ple sclerosis are extremely characteristic. Even with the 
naked eye, here and there, grayish white foci are seen in the 
brain, in the w T hite matter of the hemispheres, in the walls of 
the lateral ventricles, in the corpus callosum, in the pons, and on 



MULTIPLE SCLEROSIS. 



583 



its surface, in the medulla oblongata, in the floor of the fourth 
ventricle, and in the spinal cord, where the white matter is 
decidedly more affected than the gray. The foci are distrib- 
uted in a very irregular manner ; sometimes they are more 
numerous in the brain, sometimes they are more numerous in 
the cord, often they are found scattered equally over the en- 
tire central nervous system. If they are situated on the sur- 
face, they are seen through the pia, and are somewhat more 
prominent than the parts which surround them. They are 




Fig. 162.— Cross-section through the Cervical Enlargement of the Spinal 
Cord in a Case of Multiple Sclerosis. Hardened in osmic acid. The lighter 
colored areas in the white matter represent the sclerotic foci. (After Bramwell.) 



generally harder and firmer than the rest of the substance, and 
on section they assume a light-pink color when exposed to the 
air. If they are examined microscopically, they are found to 
consist of reticulated fibrillary connective tissue, and only con- 
tain a few intact nerve fibres ; after the death of the medullary 
sheaths, the axis cylinders are preserved for an extraordinary 
length of time (Charcot). Secondary degenerations in the 
spinal cord are often absent (Striimpell), yet they are occasion- 
ally seen (Werdnig). The vessels show an increase in the 
nuclei, later a thickening of their walls, and are seen as yellow 
dots in the sclerotic foci. Whether the disease of the vessels 
actually gives rise to the foci is not yet established (Fig. 162). 



584 DISEASES OE THE GENERAL NERVOUS SYSTEM. 

Disease of the peripheral nerves has never been demonstrated 
in multiple sclerosis. 

./Etiology. — About the aetiology we know practically nothing. 
It is possible that heredity deserves some consideration in this 
connection, but there are relatively many cases where this factor 
can positively be excluded. The influence of infectious diseases 
upon the development of insular sclerosis has recently again 
been dwelt upon by Marie (cf. lit.). Typhoid fever, variola, 
scarlet fever, measles, whooping-cough, and intermittent fever 
have repeatedly been known to precede the disease, although 
the material at our disposal is not as yet sufficient to prove a 
causative relation between the two. With regard to syphilis 
the connection here is by far less definite than, for instance, 
in tabes (cf. the case of Buss, lit.). Age and sex seem to be of 
some significance, inasmuch as children and aged people seem 
to be exempt. Westphal and others have only exceptionally 
seen it in children. Strumpell has observed it in a man of 
sixty. Both sexes seem to be attacked with about the same 
frequency. 

Treatment. — An effectual treatment for multiple sclerosis 
does not exist. We possess no remedy which will arrest the 
development of the foci. The symptomatic treatment must 
always be tried, however, and the patient particularly seeks re- 
lief from the annoying tremor. For this we may administer, 
although without raising our expectations too high, veratrine, 
physostigmine, one to three milligrammes (grs. V&rVzo) daily, in 
pills, or solanin, recently recommended by Grosset and Sarda, 
and even termed by these authors " medicament du faisceau py- 
ramidal" (Progr. med., 1888, 27). It may be given in doses of 
from two to three centigrammes (grs. %-/ 2 ) from three to five 
times daily. In other respects the treatment is the same as in 
myelitis (cf. p. 448). 



LITERATURE FROM 1884. 

Westphal. Arch. f. Psych, u. Nervenkrankheiten, xiv, 1, p. 87. (Pseudo-scle- 
rosis). 

Greiff. Ibid., 1883, xiv, 2, p. 285. 

Marie, P. Progres med., 1884, xii, 15, 16, 18. (Multiple sclerosis and infec- 
tious diseases.) 

Eulenburg. Neurol. Centralbl., 1884, 22. 

Hirt. Differentialdiagnose zwischen Hysterie und multipler Sclerose. Bresl. 
arztl. Zeitschr., 1885, vii, 11. 



MULTIPLE SCLEROSIS. 



585 



Uhthoff. Ueber Neuritis optica bei multipler Sclerose. Eerl. klin. Wochenschr., 
1885, 16. 

Koeppen. Arch. f. Psych, u. Nervenkrankheiten, 1886, xvii, 1, p. 63. (Ana- 
tomical examination.) 

Cramer, E. Ueber das Wesen des Zitterns. Aus der Krankenabtheilung des 
Breslauer Armenhauses. (Prof. Hirt.) Inaug. Diss. Breslau, 1886. 

Peltesohn. Centralbl. f. Augenheilk, 1886, p. 75. 

Moncorvo. Sulla etiologia della sclerosi a placche mi bambini e specialmento 
sulla influenza patogenica della sifilida ereditaria. Napoli, 1887. 

Gilbert et Lion. Contribution a l'etude de la sclerose en plaques a forme pr.ra- 
lytique. De la variete hemiplegique. Arch, de phys. norm, et pathol. 3me 
ser. July, 1887, p. 126. 

Unger. Ueber multiple, inselform. Sclerose im Kindesalter. Leipzig u. Wien, 
1887, Toplitz u. Deuticke. (Neurol. Centralbl., 1888, 2.) 

Oppenheim. Berl. klin. Wochenschr., 1887, 48. 

Stephan. Zur Genese des Intentionstremor. Arch. f. Psych, u. Nervenkrank- 
heiten, 1886, xviii, 3 und 1887, xix, 1. (With sixty-one references.) 

Buss. Berl. klin. Wochenschr., 1887, xxiv, 49. (Multiple sclerosis in a child 
with hereditary syphilis.) 

Hess. Ibid., 1887, xix, 1, p. 64. 

Kiewlicz. Ibid., 1888, xx, 1, p. 21. 

Bruns. Berl. klin. Wochenschr., 1888, 5. 

Gray. Boston Med. and Surg. Journ., October 15, 1888, cxix. 

Huber. Munch, med. Wochenschr., 1888, xxxv, 34, 35. 

Werdnig. Ein Fall von disseminirter Sclerose des Riickenmarkes, verbunden 
mit secundaren Degenerationen. Med. Jahrb. Wien, 1889, Jahrg. 84. 
Heft 7, p. 335. 

Uhthoff. Untersuchungen iiber Augenstorungen bei multipler Kerdsclerose. 
Arch. f. Psych, u. Nervenkrankheiten, 1889, xxi, 1. 

Charcot. Sclerose en plaques et hysteric Gaz. hebd , 1889, 2me ser., xxvi, 7. 

v. Jaksch. Wien. med. Presse, 1889, xxx, 14. 



CHAPTER II. 

TABES DORSALIS — LOCOMOTOR ATAXIA (POSTERIOR SPINAL 
SCLEROSIS — LEUCOMYELITIS POSTERIOR CHRONICA). 

The second of the diseases belonging to this group cer- 
tainly deserves to be considered as one of the most important 
of those with which we are acquainted, not only because it is 
one of those diseases of the nervous system which occur rela- 
tively frequently, and with which the general practitioner is 
not rarely brought face to face, but also because its clinical 
picture presents so many essential differences that it requires a 
large experience to feel at home with it on all occasions. No- 
body questions the importance of recognizing the disease in its 
early stages if only on account of the bearing of this upon the 
treatment, but many do not appreciate the difficulties which 
this early diagnosis entails. The more cases of tabes we see, 
the more are we surprised at the protean character of the 
symptoms, and the more are we convinced that almost every 
case offers some point of particular interest, and that occasion- 
ally even an expert can be sure of the diagnosis only after re- 
peated examinations and long observation. 

Symptoms. — The symptomatology of tabes is so compre- 
hensive that in order to get a clearer idea of it we shall sepa- 
rate the cerebral from the spinal symptoms in our description. 

The cerebral symptoms which appear in the course of the 
disease are referable either to the cranial nerves or to the 
brain substance. When the latter is affected, it is sometimes 
the cortex, at other times the white substance, and again the 
basal ganglia, which are most implicated. 

When we consider the cranial nerves, we shall find that 
there is hardly a single pair which can not be affected and 
in which lesions have not been repeatedly described in cases 
of tabes. However, not all of them are implicated with the 
same frequency, as we shall see later. The nerves supplying 
the muscles of the eye are those most commonly, the facial that 



TABES DOR SA LIS. 



587 



most rarely attacked. Between these extremes we may put 
in descending order the vagus, the optic, the fifth, the olfac- 
tory, the glosso-pharyngeal, the accessorius, the hypoglossal, 
and, lastly, the auditory. We shall take them up here in the 
order of their anatomical position, as we did in Part II. 

The lesions of the olfactory nerve possess no great practi- 
cal significance, and it is not quite certain that they are not 
more frequent than is generally supposed. They consist of a 
weakening or even a total loss of the sense of smell, or in the 
perception of peculiar, often disgusting, odors, as we have 
shown on page 25. We do not know whether these changes 
are due to anatomical lesions or only to some functional dis- 
turbances, and but little is known about the course of such dis- 
orders of the sense of smell. Occasionally, when examining 
into the condition of the sense of taste, one may accidentally 
discover an affection of the sense of smell without being able 
to ascertain how long it has already existed, as it can easily 
have escaped the notice of the patient. Only those who use 
tobacco or snuff perceive the defect very early and appeal to 
a physician for advice and help. Unfortunately, we can do 
but little. The treatment of these affections has been described 
on page 27. 

The most frequent, lesion of the optic nerve in tabes is 
atrophy or gray degeneration. Usually both eyes become af- 
fected, if not simultaneously, at least within a short time of 
each other, and it is quite rare for one eye to be diseased while 
the other remains healthy for any great length of time. The 
patients complain that everything seems as if covered by a 
gray veil. The loss of vision is particularly rapid at first ; it 
then becomes much slower, and the complete amaurosis oc- 
curs much later than one would have expected from the 
brusque onset of the trouble. Along with this, a narrowing 
(not always concentric) of the visual field appears, as the periph- 
eral portions of the retina are the first to become impaired in 
their functions. The perception for color may also be af- 
fected, as we pointed out on page 33. The order in which 
these changes occur is not always the same. As a rule, how- 
ever, the loss of color perception and the narrowing of the 
visual field precede the lessening in acuteness of the central 
vision, and it is exceptional to find diminished acuteness of 
vision and marked disturbances of color sense combined with 
a normal visual field. 



588 DISEASES OE THE GENERAL NERVOUS SYSTEM. 

The ophthalmoscopic examination shows a pale grayish 
white or bluish white, but not pure white, discoloration of the 
disk, which is thought to be produced by the obliteration of 
numerous fine vessels in the optic nerve. When the ambly- 
opia is marked but no perceptible changes in the disk are 
found, we must think of a retrobulbar degeneration of the optic 
nerve. From a pathological standpoint we are dealing with a 
degenerative atrophy, first of the medullary sheaths, and then 
of the axis cylinders. The theory that these changes are due 
to an action of the sympathetic nerves or to changes in the 
vaso-motor- nerves brought about by the spinal disease is quite 
untenable, for the process is a neuritis in which we have a 
wasting of the nerve fibres and changes in the interstitial tis- 
sue, such as have been described on page 328. 

The prognosis of the optic atrophy is altogether unfavor- 
able ; although a slight improvement or a temporary arrest of 
the process may give the patient a delusive hope of recovery, 
the termination is always in total blindness. It is true that 
the process may take several years, during which the patient 
is still able to find his way about by himself with the aid of a 
stick. 

With such a prognosis we shall not be surprised if the 
treatment is without avail. The subcutaneous injections of 
strychnine, one milligramme (grs. 1 / 6o ) twice daily in the neigh- 
borhood of the eye, as proposed by some, are of value only be- 
cause they give the patient the comforting satisfaction that 
something is being done for him, but they really have no cura- 
tive properties, and it is improbable that they even postpone 
the unfavorable issue. 

In a few isolated cases transient lachrymation has been ob- 
served (Patrolacci, These de Montpellier, 1886; Fere, L'Ence- 
phale, 1887, vii, 4). 

The nerves which supply the eye muscles — the third, the 
patheticus, and the abducens — the affections of which have al- 
ready been considered in Part II, Chapter III, frequently be- 
come attacked in the course of tabes. As a consequence of 
paralysis in the ocular muscles, one often notices diplopia, which 
may appear suddenly, and after a longer or shorter duration 
disappear as quickly. It may recur repeatedly and be a source 
of great annoyance to the patient in his daily occupations. An 
abducens paralysis may also occur by itself, and, finding this, 
one should always look for a commencing tabes, for it is fre- 



TABES DORSALIS. 



589 



quently the first sign of this disease in an apparently quite 
healthy person. If the affection remains stationary, it is to be 
regarded as being due to a nuclear lesion ; the same remarks 
apply to a ptosis which, occurring by itself, is also a suspicious 
sign, and should lead us to look for tabes. In cases of oculo- 
motor paralysis the lesion is also relatively frequently nuclear 
(page 44). 

Several of the extrinsic eye muscles may be affected at the 
same time, and an ophthalmoplegia externa is not infrequently 
observed in the course of tabes. De Watteville especially has 
directed attention to the paralysis affecting the movements of 
convergence in the initial stages of the disease. 

The behavior of the intrinsic eye muscles is not less inter- 
esting, and the condition of the pupils deserves the most thor- 
ough examination ; they are rarely normal and of the same size 
in both eyes. Frequently some abnormity of reaction is de- 
monstrable ; the marked contraction (myosis), the difference in 
the size of the two pupils (anisocoria), and the loss of the light 
reflex have already been mentioned. 

The ophthalmoplegia interna of Hutchinson, in which be- 
sides the loss of the light reflex there is also paralysis of the 
muscles of accommodation, is much rarer. The pupils of those 
afflicted with tabes may frequently be found to dilate promptly 
and normally under strong and painful irritation of the skin, as, 
for example, that produced with the faradic brush. 

The role which the affections of the fifth nerve play in this 
disease is quite subordinate ; paralytic conditions of either its 
motor or sensory branches as the result of tabes have, it seems, 
never been observed except in Westphal's case, in which there 
was degeneration of the ascending root of the fifth, and among 
the signs of irritation only the headache, traceable to the nerve 
endings in the dura, is occasionally met with. A certain rela- 
tionship is said to exist between tabes and genuine migraine, 
but in considering these cases one must make sure that the mi- 
graine has not been inherited, and furthermore note whether 
the attacks become more or less severe after the development 
of the tabetic symptoms. According to some observations, in 
such cases the headache of the migraine becomes less and 
less severe, and eventually disappears, while the nausea and 
vomiting still persist, so that it is then impossible to say 
whether we are dealing with a gastric crisis of tabes or with 
an abortive attack of migraine. In certain cases of hemi- 



59° 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



crania, if there has been, for instance, a syphilitic infection at 
some previous time, it is always well to examine carefully for 
any traces of tabes, more especially for the absence of the pa- 
tellar reflex. Occasionally one meets with a parassthesias in the 
face, the patient complaining of a sensation as if one half of the 
face and the lips were swollen ; this is probably also due to an 
affection of the ascending root of the fifth nerve. 

Lesions of the facial nerve are so rare in tabes that, when 
they occur, one can not help raising the question whether they 
are not merely to be regarded as accidental complications. 
Among two hundred and forty-seven cases of locomotor 
ataxia, I have not observed one in which any of the muscles 
supplied by the facial were affected. 

About the same may be said of the auditory nerve. There 
is no question but that lesions of this nerve may be caused 
by tabes or develop in the course of the disease, but they 
are very rare indeed ; they manifest themselves by a dimi- 
nution or a total loss of the power of hearing. The patients 
complain of deafness, which may have developed gradually or 
have come on acutely. In both cases the symptoms are due to 
organic disease of the nerve ; in the former we have to deal 
with a gradual gray degeneration of the nerve trunk, in the 
latter with a nuclear affection. Too few cases, however, of in- 
volvement of the auditory nerve in tabes have as yet been 
observed to enable us to speak with much certainty of their 
pathology (Hermet, L' Union med., 1884, 86). Under what con- 
ditions the so-called Meniere's symptoms appear in the course 
of tabes requires to be studied more closely. I have seen them 
in two of my cases, but they disappeared again in a few weeks, 
and in these cases, unfortunately, no anatomical examination 
of the internal ear could be made. 

Functional disturbances of the nerve of taste have now and 
then been described in the course of tabes. In a few instances, 
as in the case of Erben, which we considered on page 106, the 
nucleus of the glosso-pharyngeal nerve was degenerated, and 
during life such derangements of the sense of taste existed that 
the patient was at times unable to distinguish sweet things 
from those which were acid or salty. To these lesions no 
great practical significance can be attached. 

On the other hand, there is a great variety of manifesta- 
tions associated with tabes which are due to lesions of the 
vagus. In this connection we have disturbances more gener- 



TABES DOKSALIS, 



5 9 I 



ally of the digestive, but also of the respiratory and circulatory 
organs. They occur with irregularity, and may disappear 
again quite suddenly. Following the suggestion of Charcot, 
we designate them " crises." Of those affecting the digestive 
system the so-called "pharyngeal crises" are relatively the 
rarest. These consist of paroxysmal movements of degluti- 
tion, which occur from twenty to twenty-four times a minute, 
and succeed one another in this way for ten or twenty minutes ; 
the attacks may be associated with a noisy inspiration, and 
may suggest hysterical singultus ; in some cases they can be 
produced at will by pressure on the side of the larynx (Oppen- 
heim). 

The gastric crises are far more frequent ; they consist of 
paroxysmal attacks of retching and vomiting, during which 
the patient, without any particular exertion, may vomit large 
quantities of strongly acid, slimy, or watery material, after 
which he feels greatly relieved. These attacks are repeated 
for several days, sometimes for a week or two, once, twice, 
or even oftener, every day, and then disappear entirely for a 
longer or shorter period. In some cases the vomiting is asso- 
ciated with cardialgia, but usually it is uncomplicated. It is 
not at all connected with the taking of food ; indeed, it not 
infrequently occurs early in the morning when the stomach is. 
empty, and if the patient be a drinking man it may arouse a 
suspicion of the morning vomiting of drunkards. The differ- 
ential diagnosis is, however, not at all difficult ; if the vomit- 
ing be associated with vertigo, a sensation of anxiety, and a 
quickening of the pulse, it can not be considered simply as a 
"gastric crisis." This paroxysmal vomiting is of the great- 
est importance for the diagnosis of tabes. It is frequently re- 
garded as dependent upon some stomach trouble and treated 
as such for a long period without any sign of improvement, 
until finally, perhaps by accident, our attention is drawn to 
some other symptom which places the diagnosis beyond doubt. 
If a person have paroxysmal vomiting and complain occasion- 
ally of violent rheumatoid pains in the legs, we should examine 
most carefully for tabes, and we shall frequently be surprised 
at the ease with which we can make the diagnosis, and wonder 
that we had ever been under the impression that the patient 
had simply " chronic gastritis " and " rheumatism." The state- 
ment of Eckert (Die intestinalen Erscheinungen der Tabes. 
Inaug. Diss., Berlin, 1887) that gastric crises must be divided 



cq2 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

into those of central and those of reflex origin deserves to be 
investigated more closely. In the central form he assumes, 
besides a general condition of irritation in the brain, some 
affection of the nucleus of the vagus, in the reflex form a pe- 
ripheral irritation of the vagus which, under certain circum- 
stances, may be produced by the ingesta. He holds that in 
the latter cases the vomiting is not associated with any dis- 
tressing nausea, so that the patient suffers relatively little. 

Sometimes intestinal disturbances manifest themselves by in- 
tense "lightning" pains about the rectum and anus, the "anal 
crises"; in other cases by tenesmus, which forces the patient 
to go frequently to stool, though he is able to pass little or 
nothing ; and, lastly, by the so-called tabetic diarrhoea, about 
the causation of which we are absolutely ignorant. This diar- 
rhoea may be more or less persistent, and be followed by an 
equally protracted and obstinate constipation. Incontinence 
of faeces is rarely present, though on rectal examination we 
shall occasionally discover sensory disturbances, particularly 
anaesthesia of the mucous membrane. Paresthesias may also 
occur, and the patient may experience a sensation as if he had 
a foreign body in the rectum. 

By " laryngeal crises " we mean those paroxysms of dysp- 
noea which may occur when the patient is lying down, or, in 
other cases, only when he attempts to move or walk about. 
Sometimes they appear in the form of peculiar suffocative at- 
tacks, accompanied by violent coughing, and are often pre- 
ceded by a sighing or whistling inspiration. These attacks 
may last several minutes, during which the suffering may be 
so intense that the patient gives up all hopes of recovery. 
Attacks of even moderate intensity, in which a long, sonorous 
inspiration follows several short expirations, are most disagree- 
able for the patient, and appear very serious ; under some cir- 
cumstances they may be mistaken for whooping-cough. These 
crises are caused by changes of temperature, speaking for a 
long time, or by strong odors, smoking, etc. The result of the 
laryngoscopic examination is frequently negative ; in other 
cases one finds paralysis of some of the laryngeal muscles ; 
here also, in all probability, we should distinguish a central 
and a reflex form. 

Abductor paralysis — i. e., paralysis of the muscles that open 
the glottis — sometimes occurs among the early signs of tabes, 
and may lead to serious danger of suffocation ; but we are 



TABES DORS A LIS. 593 

unable to say whether this should be attributed exclusively to 
paralysis of the abductors, or to spasm of the adductors alone, 
or to both conditions. We may consider the condition de- 
scribed by Gray (Brain, January, 1888), in which the voice 
often breaks and takes on a high falsetto, as a kind of " laryngeal 
ataxia." 

Attacks of angina pectoris, with all its characteristic symp- 
toms, are rarely met with in tabes, though Vulpian, among 
others, has seen them (Revue de med., 1885, v > 0- 

Lesions of the accessorius are considered as rarities in the 
course of tabes. In a case observed by Martius (cf. lit., page 
141) there was an atrophic paralysis of the upper portions 
of both trapezii, while the sterno-cleido-mastoids, which also 
receive fibres from the cervical plexus, were not affected. 
Whether, and if so under what circumstances, one or both of 
the two nuclei of the accessory nerve are affected (the nucleus 
accessorius vagi and the nucleus spinalis) we are absolutely 
ignorant. It is also uncertain whether symptoms of irritation 
in the domain of the accessorius — e. g., torticollis — do occur in 
the course of tabes. 

Among the lesions of the hypoglossus there is one which de- 
serves a special mention in this place— that is, the hemiatrophy 
of the tongue described above, which Ballet (lit., page 148) 
stated was relatively often observed. He even went so far as 
to say that, when one found this hemiatrophy, tabes should 
always be suspected. We can only agree with him to a lim- 
ited extent. We have certainly found hemiatrophy in cases 
of tabes, but we must remember that it is in itself a rare affec- 
tion, and that it exists more often independently than associ- 
ated with tabes. In addition to the two cases which we men- 
tioned on pages 146 and 147, we desire to record another (Fig. 
163), in which there was likewise no trace of locomotor ataxia. 
It seems that the hypoglossal nucleus is not very liable to the 
degenerative processes of this disease. 

Cerebral disturbances of the most manifold variety appear 
in the course of tabes, and we would in the first place call 
attention to the paroxysms of vertigo which come over the 
patient when he looks up or makes quick movements of the 
head, and which impel him to seize the nearest object to pre- 
vent himself from falling. There may also be found psychical 
depression and a feeling of dread and anxiety, which in some 
cases may be followed by well-marked psychoses. Among 
38 



594 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



the not very rare forms of psychoses in this disease we may 
mention paranoia, melancholia, and simple dementia ; but far 
more frequent and important than all these taken together is 
the progressive paralysis of the insane, which very frequently 
accompanies tabes. But here we must try to make out which 
of the two affections was the first to develop, for in some in- 
stances the tabes precedes the paralysis, while in others the re- 
verse is the case. The process can extend from the brain to 




Fig. 163.— Hemiatrophy of the Tongue in an otherwise perfectly Healthy 
Child (personal observation). 

the cord or from the cord to the brain, as the case may be, and 
Westphal was certainly justified in making the statement that 
" in certain persons there is a peculiar disposition of the nerv- 
ous system, and that this, under the influence of different excit- 
ing causes, the action of which we do not understand, expresses 
itself in the form of affections either of the spinal or cerebral 
portion of the nervous system or of the peripheral cranial 
nerves, the different affections occurring in some cases nearly 
at the same time, in other cases at varying intervals." 

Epilepsy occurring in connection with tabes has already 



TABES DORSALIS. 



595 



been considered in the chapter on the former disease. On this 
subject Schlieper, working under my direction, has published 
an article (Inaug. Diss., Breslau, 1884). 

The cases of hemiplegia which occur in the course of tabes 
are mostly of the indirect variety — that is, they disappear in a 
shorter or longer time — and do not owe their origin to the 
rupture of vessels or to lesions of the internal capsule. The 
face is usually only slightly affected, and that only for a short 
time, and the extremities are not wholly paralyzed, but are 
only in a paretic condition, which usually disappears without 
any sort of treatment. 1 have repeatedly seen such cases of 
hemiparesis come on without any warning and with only a 
slight disturbance of consciousness and entirely disappear in 
a relatively short time. A. Bernhardt (Archiv f. Psych, u. 
Nervenkrankheiten, 1883, xiv, 1) has recorded instances in 
which they were accompanied by aphasic conditions. 

So great importance has been attached to the spinal symp- 
toms that they usually occupy the greater part of all descrip- 
tions of the clinical history of the affection, and have been 
allowed to predominate so far, that all other symptoms have 
been treated of as being of little importance and as if the only 
lesion was that in the spinal cord. And still, it is not rare to 
meet with cases in which the spinal symptoms have been for a 
long period of very little importance, and with a few, in which 
they have never attained to any prominence, while the major- 
ity of the troublesome symptoms were due to affections of the 
brain and its nerves, and the lesions of the peripheral nerves 
gave rise to more marked symptoms than those of the spinal 
cord. Observations of this kind, the number of which will be 
rapidly increased by conscientious examinations, go to show 
that the entire nervous system participates in the morbid pro- 
cess, and to consider this participation to be the rule is abso- 
lutely necessary for a correct comprehension of the pathology 
of this disease. 

The symptoms produced by the spinal lesions concern mo- 
tility, sensibility, and the reflexes. 

The disturbances of motility are manifold ; they depend 
partly on a decrease in the strength of the muscles, partly on 
disturbances of co-ordination. The first is not very common ; 
on the contrary, one can frequently observe that the mere 
strength in the extremities has not been at all affected, and 
yet the motility has suffered. This condition depends, then, 



596 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

upon a faulty co-ordination, and is broadly designated as 
"ataxia." Movements, such as walking, writing, taking hold 
of an object, etc., for the proper execution of which the simul- 
taneous working together of several muscles is necessary, are 
designated as " co-ordinated." For such movements more than 
a simple innervation of the muscles is requisite ; it is necessary 
that each concerned should receive, so to speak, the proper 
amount of innervation and at the proper time, so that the 
contraction of the various muscles may take place at the right 
moment. It is only when all these various factors are prop- 
erly combined that the movement is correctly executed, and if 
one of them be disturbed the entire movement becomes ataxic. 
Even if not pathognomonic, it is certainly very characteristic 
of tabes that in the later (rarely in the earliest) stages, certain 
movements become ataxic, particularly those of the lower ex- 
tremities, and, above all, the gait. Such abnormities are met 
with much less frequently in the upper extremities, and the 
movements necessary for writing, handling a spoon in eating, 
and the like, usually remain normal. 

The gait of a tabetic is readily recognized even by one who 
has had little experience in that direction ; one notices particu- 
larly that the patient exerts his eyes almost as much as his feet, 
that he watches every step, and in passing over small obstacles, 
as for example a curbstone, determines exactly where he must 
place his foot. If he ceases to use his eyes in this fashion for 
any reason, even for a short time, the movements of the legs 
become uncertain, and he is in danger of falling. But not even 
with the help of the eyes can he walk without difficulty. He 
does not step out in the usual way ; the legs are thrown out 
loosely, and in putting the feet to the ground the heels come 
down first (" strutting gait "). The manner in which the feet 
are raised, the legs thrown out, the stamp with which the feet 
touch the ground, readily enable one to diagnosticate the ta- 
betic gait at a distance, and we shall seldom make a mistake if 
we consider a person who walks in this manner, supported on 
a stick or by an attendant, as affected with locomotor ataxia. 
Acts of politeness, such as greetings and stopping to talk on 
the street, do not afford these persons much pleasure, for they 
distract their attention, which has to be kept undivided if they 
would walk in safety. 

The uncertainty and insufficiency of the innervation of the 
different groups of muscles is apparent not only in the walk, 



TABES DOR SA LIS. ^j 

but even while the patient is standing still. He is not able to 
stand up straight without tottering, particularly when he closes 
his eyes, and he sways to and fro and falls unless some one is 
at hand to support him (" Romberg's sign "). The smaller the 
supporting basis — that is, the nearer together the feet — the more 
pronounced does the phenomenon become. In some cases it 
may be accompanied by irregular contractions of the calf mus- 
cles. 

The much rarer ataxia of the upper extremities produces 
inability to write, to play the piano, to sew, etc. With closed 
eyes the patient is unable to describe circles in the air with his 
arms, to bring the tips of the index fingers together from a dis- 
tance, or to touch the end of the nose quickly with his finger. 
All such movements are carried out with more or less irregu- 
larity. It is exceptional for the upper extremities to become 
affected at an early period or severely ; as a rule, we can not 
detect ataxic movements in them in the earlier stages, and when 
they do occur they can, at least in some instances, be traced to 
some special cause. In the case of Bernhardt (Zeitschr. f. klin. 
Med., 1888, xiv, 3, page 289) they were due to the occupation 
of the patient. Remak (Berlin, klin. Wochenschr., 1880, 22) has 
also published a similar case of ataxia affecting only the upper 
extremities. It was associated with ephidrosis unilateralis. The 
helplessness of the patient reaches the most extreme degree 
when the ataxia affects all four extremities, as in the case of 
Fort (Dublin Journal of Medical Science, 3, s., 1886, clxxiii). 

But we must also distinguish between spinal and cerebral 
or the so-called cortical ataxia (page 184). A conclusion im- 
portant for the differential diagnosis may be drawn from ob- 
serving the influence which the eyes exert over the co-ordi- 
nated movements. In spinal ataxia these become better regu- 
lated and more certain when they are under the control of the 
eyes, while in cortical ataxia such a control has no influence. 

The physiological cause of ataxia is not as yet positively 
known, but even to-day is a source of contention and still the 
object of continued investigations. While some, as Benedikt, 
Cyon, and Jaccoud, consider that we have to do with a disturb- 
ance of the reflex activity in the cord, others, with Friedreich, 
and after him Erb, are of the opinion that there is a disturbance 
in co-ordinating fibers, the course of which they confess can 
not as yet be made out. Thirdly, others, with Leyden at 
their head, consider disturbances of sensibility to be responsi- 



598 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



ble for the ataxia. According to these, interruption of con- 
duction in the sensory tracts of the gray matter causes a break 
of the reflex arc between the sensory nerves of the muscles 
and the motor nerves. "Owing to this interruption, the un- 
conscious regulation of the movements, which adapts them 
to the state of contraction or relaxation of the musculature, 
disappears" (Wernicke), and ataxia is the result. This "sen- 
sory ataxia " has always had many opponents, for one was 
obliged to confess that ataxia often occurs when no sen- 
sory changes are found ; but in spite of this fact some one is 
constantly returning to this theory, which has lately found an 
advocate in Goldscheider. In a comprehensive article (Zeit- 
schr. f. klin. Med., 1888, xv, 1, 2) he subjects the meaning of the 
term "muscular sense" to a fresh examination, and comes to 
the conclusion that four factors are combined in the formation 
of the muscular sense, viz. : (1) the sensibility to active, (2) to 
passive movements, (3) the perception of position, and (4) the 
perception of weight and resistance. He then states that in 
all cases of ataxia in which the sensibility had been tested the 
examination had been imperfect in some detail ; he pointed out 
that, for example, in the otherwise admirably conducted ob- 
servations of Friedreich, the examination of the sensibility to 
movement had been omitted. According to his view, there- 
fore, it is only necessary to perfect the examination of the 
sensibility in order to come to the conclusion that sensory dis- 
turbances are responsible for the ataxia. 

When one considers that we are ignorant of the origin of 
the normal co-ordination, and remembers that it is not congeni- 
tal but must be learned by practice, in which controlling and 
correcting influences, which arise from the periphery, come 
into play, it is not difficult to agree with Striimpell, who con- 
siders that the ataxia takes its origin from the disappearance 
or insufficiency of those regulating influences, because "the 
possibility of successfully transferring them to the motor ap- 
paratus is removed " (Nervenkrankheiten, Aufl. iv, pages 209, 
210). We should then have to regard the gray substance and 
the ganglionic cells as the place where this transfer probably 
occurs. Which of the theories above mentioned will at last 
be recognized as the correct one, and whether or not other 
factors, which have not yet been considered, play a part in the 
production of the ataxia, it is at present impossible to state. 

Later on in the course of tabes there is a diminution in the 



TABES DORS A LIS. 



599 



actual strength of the voluntary muscles, particularly in those 
of the lower extremities. This first manifests itself by wea- 
riness on walking, which gradually increases, and finally ends 
in total paralysis (paraplegia). The patient first notices that 
he has to rest in the course of walks which he previously 
was in the habit of taking without any feeling of fatigue, that 
it takes him much longer than formerly to cover a particular 
distance, and that he is in general unable to take the exercise 
to which he was formerly accustomed. As the disease advances, 
the power of locomotion becomes more and more diminished, 
and the patient is only just able to drag his legs along, and 





Fig-. 164. — Specimen of Handwriting in a Case of Tremor in Tabes (personal ob- 
servation). 

at last, becoming unable to move at all or even stand without 
help, is obliged to spend the rest of his life in the invalid's 
chair. 

Signs of motor irritation are rare and are limited to parox- 
vsmal twitchings in the fingers and toes; sometimes, however, 
involuntary movements occur in the limbs which the patient 
has absolutely no intention of moving. Stintzing (Centralb. f. 
Nervenheilk., 1886, 9, 3), for example, observed an involuntary 
flexion of the hip joint when the patient coughed. Similar 
associated movements in the fingers or toes have been de- 
scribed by Striimpell (Neurol. Centralblatt, 1887, vi, 1) and 
Oppenheim (Sitzung der Charite-Gesellschaft, 20 M'arz, 1884). 

The athetoid and choreiform movements described by 



600 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Andry (Revue de med., 1887, 1), sometimes found in tabetics, 
are to be regarded as due to simultaneous disease of the lateral 
columns, and accordingly rather as complications. We must 
regard the tremor as one of the signs of motor irritation, al- 
though we are at present unable to localize its anatomical seat. 
This symptom is sometimes observed either in the initial stage 
or in the further course of the disease. If the upper extremities 
become affected by it, the handwriting is altered, in the man- 
ner represented in Fig. 164. 

The disturbances of sensibility in tabes are either experi- 
enced subjectively by the patient, or can only be discov- 
ered by an objective examination. Their number is exceed- 
ingly large, and it is safe to say that in almost every case some 
interesting observation of this character may be made. Symp- 
toms of irritation alternate with those of paralysis, and one 
also meets with other different disturbances of sensation which 
belong to neither of these groups, and which are more variable 
in tabes than in any other affection. 

Among the subjective symptoms we shall consider first the 
symptoms of irritation, more particularly the pains, which in 
the life of tabetics play such an important part. They, too, 
are of a changeable nature, and vary considerably in their 
situation and intensity. In the first place we desire to direct 
attention to the muscular pains, which, if they do occur at 
all, occur very early in the course of the disease, and affect 
sometimes the shoulders and sometimes the legs, and recall 
the well-known muscular pains which follow marked exer- 
tion in the gymnasium, mountain climbing, rowing, etc. As 
a rule, it is true, they are not very intense, but when they 
•come on suddenly, without any appreciable cause, the patient 
is obliged to remain perfectly quiet for several hours, for every 
motion is difficult to him, and if he persists in his attempts, 
movement becomes impossible on account of the feeling of 
weakness and fatigue which at last overcomes him. Pitres 
calls these pains "crises de courbature musculaire " (Progr. 
med., 1884, xii, 28), and considers that they are precursors of 
tabes. 

We must separate from these the nervous pains of tabetics 
which are dependent upon irritation of the posterior roots. 
They are usually situated in the lower extremities, and manifest 
themselves either as dull, boring sensations, or as sharp pains 
which last for hours and then disappear for a time ; they may 



TABES DORSALIS. 6oi 

also be felt in the back and sacral region, and for years be 
attributed to rheumatism, lumbago, etc. As long as only these 
pains exist, the life of the patient is bearable, although it may 
be marred and his occupation interfered with, but there is a 
second class of nervous pains which, appearing and disappear- 
ing like lightning, are known as shooting or lancinating pains, 
" douleurs fnlgnr antes." It is these that make the existence of 
the tabetic most miserable, and make him wish that he were 
dead ; it is these, again, that can reach an intensity which 
causes the most resolute sufferer to lose his energy, and con- 
verts him into a complaining and whining weakling. They 
also occur paroxysmally, and may continue for minutes, hours, 
or even days, and then disappear for variable periods, some- 
times for months. In many cases they recur often, some- 
times every week, but they then usually only last for a few 
moments. 

In some cases, in connection with these attacks, cutaneous 
ecchymoses may develop, which are to be noted in the por- 
tions of the body subjected to the pain, and may attain a con- 
siderable size, so that one who does not know their significance, 
on examining the patient, may come to the conclusion that he 
had been injured by a blow or a fall. In still rarer instances 
swellings have been observed instead of the ecchymoses, which 
in the same manner as the latter disappear in a few days. 

Along with these pains the patient may suffer with hyper- 
esthesias of the skin to such an extent that in certain parts of 
the body — very frequently, for instance, on the back — he can 
not bear the slightest pressure, and even his clothes will be a 
source of annoyance to him. These cutaneous hyperesthesias 
may persist for months unchanged without being affected in 
the least by the paroxysmal pains. 

Among the symptoms of sensory irritation the so-called 
girdle sensation may also be reckoned. This likewise occurs 
paroxysmally, at which times the patient experiences a feeling 
as if a belt were being drawn around his chest and abdomen, 
which interferes with his breathing. 

Manifestations of sensory paralysis may also be subjectively 
perceived by the patient. Not infrequently he will say that 
he does not feel the contact of the clothing on certain portions 
of the body, or that the soles of the feet are without sensation. 
In a case under my observation the patient complained of a 
widespread loss of sensation in the perineal region, which on 



6o2 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

objective examination proved to be anaesthetic as well as the 
inner surfaces of both thighs. To the anaesthesias, which are 
particularly unpleasant to the patient, belong those affecting 
the mucous membranes — as, for example, that of the rectum — 
owing to which the bowel may empty itself without the patient 
being conscious of it. Again, there are anaesthesias of the 
mucous membrane of the sexual organs — as of the vagina, for 
example — owning to which the pleasurable sensations attending 
coitus are either absent or greatly diminished. 

Among the perverted sensations which are experienced 
subjectively may be mentioned the alterations of feeling in the 
soles of the feet, owing to which it appears to the patient that 
he is not walking upon solid ground, but rather upon a soft, 
yielding surface, such as moss, cotton, etc. To these may be 
added the sensation as of ants crawling over the skin, a feeling 
of numbness, which usually appears in the lower extremities, 
but sometimes also in the hands. In the latter case it may 
become impossible for the person to write, sew, etc., in spite 
of the fact that he may be suffering from no disturbance of 
motility whatsoever. 

Many anomalies of sensation in tabes can only be discov- 
ered by means of objective examination. They constitute the 
second group of sensory disturbances to which we referred 
above. 

We would here insist upon the necessity of making the 
examination as carefully as possible, and of remembering in 
the first place that when the patient is repeatedly examined he 
ceases to give us his attention and makes careless answers to 
the inquiries made of him, and in the second place that there 
are certain sensations, the so-called spontaneous sensations, 
which the patient experiences without any external irritation 
whatever. Rosenbach (Deutsch. med. Wochenschr., 1889, 13) 
holds that accumulations of weak sensory stimuli occur, the 
intervals between which vary according to the strength of the 
stimuli and the better or worse condition of the patient. 
If one remembers this and the fact that the so-called after- 
sensations must also be taken into account when making the 
test, one will be able to avoid gross errors. B. Stern (Arch. f. 
Psych, und Nervenkrankheiten, 1886, xvii, 2) has not been able 
to confirm the statement of Belmont (Gaz. med., 1877, 19) that 
points of predilection exist for the disturbances of sensation in 
tabetics, as, for example, in the soles of the feet, the area about 



TABES DORSALIS. 



603 



the malleoli, and the lower extremities in general. Were it 
true, it might constitute a new source of error in the examina- 
tion of the anomalies of sensation. The methods of examina- 
tion are as simple as possible, and the necessary instruments 
are an induction apparatus, Weber's assthesiometer, needles, 
mounted brushes, and test tubes filled with hot and cold water. 
With these one is able in most cases to obtain all the necessary 
information. 

Among the symptoms of irritation, hyperesthesias, as we 
stated above, are not of very frequent occurrence, but when 
they do occur they can very easily be recognized. They are 
frequently quite transient, so that a point, which yesterday was 
sensitive to the slightest touch, presents to-day a perfectly nor- 
mal condition. The exaggerated sensitiveness is probably al- 
ways confined to the perception of pain, but is not found asso- 
ciated with the other qualities of sensation. We recognize 
another symptom of irritation in the so-called double percep- 
tion of painful impressions, polyassthesia (Fischer), by which 
we mean that from one external irritation, as the prick of a 
needle, the patient experiences two painful sensations in suc- 
cession. 

In the objective examination of the sensibility the symptoms 
of paralysis play, without doubt, the more important role. In 
the first place there are the anaesthesias, which may affect all 
qualities of sensation, the sense of pain, touch, and temperature. 
The most interesting is an analgesia, to which Berger first 
directed attention, who demonstrated that while the patients 
reacted normally to slight stimuli, they scarcely did so at all to 
stronger ones. We must consider it as an anomalous analgesia, 
when a patient experiences only one kind of pain in response to 
the most varied kinds of painful stimuli. It sometimes happens 
that the tabetic can not tell the difference between the action 
of the thermo-cautery, the simple prick of a needle, or a violent 
pinch, and designates the pain produced by these various 
agents as simply a burning one. The painful sensation on elec- 
trical stimulation may also become abolished, so that we can 
apply the strongest currents or the faradic brush to the most 
sensitive parts, such as the inner surfaces of the thighs, the pe- 
rinaeum, or the scrotum, and the patient not give the slightest 
evidence of pain. 

Lastly, delayed sensation is to be considered as a symptom 
of a paralytic nature. In these cases, when the patient is 



604 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



pricked with a needle, he does not experience pain until one, 
two, or three seconds later. The delay of perception may 
vary for the different qualities of sensation — for example, for 
touch and pain — as Osthoff and Remak have pointed out. 

We must attribute to disturbances of the muscular sense, 
which we alluded to in discussing the cause of ataxia, the fact 
that the patient with his eyes closed is unable to state accu- 
rately in what position his extremities are, and if one, for in- 
stance, changes the position of a limb, he is not at all certain 
into what position it has been put. He is unable to estimate 
the weight of an object placed in his hands, and so forth. All 
these conditions are to be remembered when one is testing the 
muscular sense, and at the examination one will have to ascer- 
tain what is the minimum change of position which can still be 
recognized by the patient. 

Of the disturbances of the reflexes, those of the skin inter- 
est us less than those of the tendon reflexes ; of the latter, the 
patellar reflex is the most important, the anatomical localiza- 





Fig. 165.— Two Cases of Tabes. (After Westphal.) 

A. The lines hh show the limits of the so-called "root zone." The degeneration is progress- 

ing from within toward them, but only reaches the border line. The patellar reflexes 
were retained until death. 

B. The degeneration is progressing from within outward, and has extended far into the 

" root zone." The patellar reflexes were lost five years before death. 

tion for which is in the so-called root zone (Westphal). This 
zone is situated at the junction of the lower dorsal portion of 
the cord with the lumbar enlargement at the level of exit of 
the second, third, and fourth lumbar nerves (cf, page 420), and 
constitutes the area which the roots entering to the median side 
of the posterior horn must traverse in order to reach the 
substantia gelatinosa of the posterior horn. If this field is de- 
generated, then the patellar tendon reflex disappears, but if it 



TABES DOR SA LIS. 605 

is normal, the reflex is preserved (cf. Fig. 165, A and B). The 
rare cases in which it remains preserved on one side also con- 
firm the localization assumed by Westphal ; at the autopsy it 
has been repeatedly noted (cf. Berlin, klin. Wochenschr., 1887, 
31, page 586) that there was a degeneration of the posterior col- 
umns and of the "root zone " on the affected side, while this 
zone on the healthy side was intact. 

The disappearance of the patellar reflex, " Westphal's sign," 
was formerly considered as pathognomonic of tabes, and when- 
ever the knee jerk could not be obtained, the diagnosis was 
made without hesitation. This was the standpoint taken in 
the earlier works of Westphal, Erb, and others, and it must be 
confessed that " Westphal's sign " is observed in by far the 
greater number of cases of tabes, and usually early in the 
course. However, it began to be doubted that the rule was 
without exceptions, and toward the end of the seventies sev- 
eral undoubted cases of tabes were reported (Berger, Fournier) 
in which the patellar reflex was retained to the end of life, and, 
since then, other similar cases have been added. Westphal 
himself pointed out that the knee phenomenon might persist 
with degeneration of the posterior columns (Arch. f. Psych, 
und Nervenkrankh., 1886, 17, 2), and precisely at this time I 
myself reported two such instances (Berlin, klin Wochenschr., 
1886, 10). Accordingly, it is an undeniable fact, and one 
which, anatomically, can be readily explained, that under cer- 
tain circumstances— that is, whenever the " root zone " remains 
free from degeneration — the patellar reflex may continue to be 
present during the entire course of the disease. By repeated 
and accurate examination, in which Jendrassik's method of re- 
enforcement should not be forgotten, one is sometimes able to 
follow up the gradual disappearance of this reflex, and to ob- 
serve that the time of its diminution and final disappearance 
may differ in the two legs — for example, the reflex may still be 
well marked on one side, while it has completely disappeared 
on the other. Among others, Goldflam has reported observa- 
tions on this point (Neurol. Centralblatt, 1888, 19), and has sup- 
posed that interference with conduction, produced by patho- 
logical changes in the peripheral nerves, may also be the cause. 
The patellar reflex which has once disappeared in the course of 
tabes can never reappear, since destruction of the correspond- 
ing portions of the cord has taken place, but in traumatic neu- 
roses this may very well happen, and in doubtful instances it 



606 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

may become an important point in the differential diagnosis. 
The patellar reflex can only be increased in tabes when there 
is a coincident degeneration of the lateral columns. 

While, then, for the reasons we have given, " Westphal's 
sign " can not be regarded as pathognomonic, there are still 
others which should warn us against laying too much stress 
on the condition of the patellar reflex in the diagnosis of tabes. 
Unquestionably it may also disappear under certain circum- 
stances in the course of other affections — as, for example, in 
certain diseases of the brain — if the muscular tone necessary to 
its production has been lost ; also in neuritis, poliomyelitis, 
diabetes, chronic alcoholism, and in affections of the knee 
joint when the movements of the tendon are interfered with. 
When we add that it can not be demonstrated in all healthy 
persons — a small number being entirely without it, as Berger 
and others have stated — and moreover consider the fact that 
in old age and in conditions of marked nervous exhaustion it 
may entirely disappear without any apparent reason, perhaps 
from a diminished tone in the muscles, we shall have sufficient 
grounds for not overestimating its significance, important as 
it may still be for the recognition of tabetic processes. The 
measurements of its strength, which have lately been made a 
good deal of, may for the present be omitted in practice with- 
out disadvantage for the diagnosis. 

The reflex centres for the functions of the bladder, rectum, 
and sexual apparatus, which are situated in the lumbar portion 
of the cord, are naturally also greatly disturbed in the course 
of tabes. The reflex processes, which come into action here, are 
but little understood, but their pathological condition has been 
studied with great care. Much attention has been directed 
toward the bladder troubles of tabetics, and attempts have 
been made to distinguish between the different kinds of affec- 
tions. They are motor or sensory, or both, according as only 
the one or the other or both centres have been destroyed by 
the degenerative process in the cord. 

Among the motor disturbances there are symptoms of irri- 
tation as well as of paralysis, which may affect equally the 
sphincter and the detrusor, so that the will may have but little 
influence over them, or finally none at all. According as one 
or the other condition is the more prominent, the complaints 
of the patient differ ; sometimes he is obliged to strain for a 
long time before the bladder will begin to empty itself, and 



TABES DORSALIS. 



607 



even then the stream is often interrupted ; sometimes he is 
unable to urinate at all in the erect posture, but must squat 
down or sit on the closet to bring the abdominal muscles into 
action in order to expel even a few drops of urine, and the act 
of micturition may take so long, that the patient feels ashamed 
to use the public conveniences. In other cases, where there is 
not only paresis of the detrusor, but at the same time a spasm 
of the sphincter, the patient can not urinate at all, and the re- 
tention must be* relieved by means of the catheter ; in other 
instances, again, where there is a paresis of the sphincter, he 
has to urinate very frequently. Long before the bladder is 
full — every hour or two — he feels an irresistible desire to empty 
it, which he must satisfy or run the risk of an involuntary pas- 
sage of urine. He is unwilling to go upon railroad journeys, 
to go into society, to lectures, or to the theatre, for fear that 
he will not be able to reach a convenient place in time where 
he can urinate in peace. Paresis of the sphincter is often a 
reason why the patient sleeps poorly, because he has to get up 
so often to urinate, and if he sleeps soundly he does not appre- 
ciate the calls of Nature, and will pass his urine in bed. When 
he coughs or sneezes the under-garments are moistened with 
urine, and, despite his utmost efforts, he is unable to prevent 
it. In the more marked degrees of weakness of the sphincter 
there is an involuntary trickling or an occasional discharge of 
urine, which the patient is unable to predict ; this necessitates 
the constant wearing of some sort of receptacle ; otherwise 
the patient is surrounded by such an ammoniacal odor that the 
incontinence is recognizable without any examination. If there 
is a combination of retention and incontinence, it manifests it- 
self in the following manner : After long straining the urine is 
passed in a moderately strong stream, but this suddenly ceases, 
and can only be started again after renewed efforts. Some- 
times, after the patient has strained in vain for a long time and 
has given it up in despair, the urine is passed involuntarily. 
These and many other facts of the same description are only 
to be discovered after careful and repeated questionings and 
examinations. 

Sensory disturbances may manifest themselves (1) by more 
or less intense pain before and during the act of micturition, 
which may distress the patient greatly and make him dread to 
relieve his bladder (the " crises vttsicales " of Charcot). The 
pain may be situated either in the hypogastric region or ex- 



6o8 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



tend down into the urethra {crises vesico-ure'tkraZes). Painful 
strangury, forcing the patient to urinate every half hour, when 
he only passes a few drops, has also been observed. On the 
other hand, (2) there may be a diminution in sensibility, so 
that, in consequence of the anaesthesia of the mucous mem- 
brane of the bladder and urethra, the flow of urine is not no- 
ticed, and the patients, especially when there is a weakness of 
the sphincter at the same time, do not know whether they are 




Case of Charcot's Joint in a Tabetic (personal observation). 



urinating or not, and only become aware of the fact when they 
feel the chilly sensation proceeding from the damp clothes. A 
rather rare manifestation, which may be observed after violent 
bladder crises, is the appearance of hasmaturia, which must be 
attributed to capillary haemorrhages into the bladder or ure- 
thra; the bloody character of the urine may be a source of 
new anxiety and worry to the unfortunate patient, already 



TABES DORSALIS. 



609 



greatly broken down by the agonizing pains. These hemor- 
rhages may be considered as analogous to the ecchymoses in 
the skin occurring after the intense lancinating pains, which 
we mentioned above on page 601. 

The most troublesome rectal symptom is the very obsti- 
nate constipation. Incontinentia alvi and anaesthesia of the 
rectal mucous membrane, in consequence of which the patient 
is not aware of the act of defecation, and so soils himself un- 
consciously, are among the rarer occurrences. 

The centre for the sexual functions, the seat of which is 
also in the lumbar enlargement, is not only under the control 
of reflex, but also of cerebral influences. If the path coming 
from the psychical centres is interrupted, the performance of 
the function is faulty ; if the path from the inhibitory centres is 
disturbed, the sexual reflex activity is increased and priapism 
may occur. Pitres (Progr. med., 1884, xii, 37), under the name 
of " crises clit.oridiennes" has described in women conditions 
which consisted of periods of voluptuous excitement accom- 
panied by secretion, analogous to the violent erections and 
spermatorrhoea found in men in the initial stages of tabes. 
Such cases are, however, at least in Germany, exceptional. 
Not infrequently tabetics have been known to preserve their 
virility, and even after the beginning of the disease to beget 
one or even several healthy children. Only later does the 
sexual power, and with it the desire, become diminished, and 
coitus lose its charm, so that it is undertaken more rarely, the 
act being sometimes incomplete. A normal condition of the 
nerves necessary for the erection of the penis, associated with 
a paralysis of those going to the ejaculator seminis, so that 
while coitus and orgasm are normal, the semen is not emitted 
till later, and then very slowly — a condition which Bernhardt 
has observed after injury (Deutsch. med. Zeit., 1888, 48) — has 
been known to occur also in the course of tabes. 

The vaso-motor and trophic centres in most cases are not 
affected. In the majority of instances, symptoms* of this char- 
acter are entirely absent during the whole course. In some, 
however, peculiar symptoms attract our attention, as, for ex- 
ample, a local hyperidrosis, which Ollivier (Gaz. hebdom., 
September 7, 1883, xxx > 3 6 )> Raymond and Arthaud (Revue de 
med., 1884,4, 5)> an d others have observed on the hands and 
feet. In a case of tabes we have also seen the sweat secretion 
on the hands so increased that we were able to note the forma- 
39 



610 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

tion of small drops and watch them unite to form a steady- 
dripping. In another case there was unilateral sweating, the 
hyperidrosis appearing after every meal on the left half of the 
head, face, and neck. I do not care to risk an opinion as to 
how far an assumption of an affection of the sympathetic would 
here be justifiable. 

Greater practical importance must be attributed to the 
changes which are observed in the nails and teeth of those af- 
fected with tabes. The nails are either deformed, becoming 
twisted or marked by deep furrows, or fall out entirely from 
the ringers as well as from the toes, as Joffroy (L'Union, 
1882, 106), Bonieux (These de Paris, 1883, No. 237), Hay-Mar 
girandiere (These de Paris, 1883, No. 75), and others have ob- 
served. The loss of the nails (" la chute des ongles") is not rare 
in tabes, and is in some cases to be attributed to the temporary 
cessation of growth of the nail matrix. In others an ecchy- 
mosis under the nail may be the exciting cause. Under cer- 
tain circumstances the nail of the great toe falls off altogether, 
without pain, with only a slight itching sensation, and the 
newly formed nail, which is often rough and irregular, soon 
shares the fate of its predecessor. 

It is occasionally observed that the teeth become loosened 
without any pain and fall out without the appearance of any 
symptoms of inflammation, the tooth itself being intact. This 
arises from some disturbance in the nutrition of the jaw, a rare- 
fying ostitis which is connected with a lesion of the nucleus of 
the trigeminus (Vallin and Demange). In this way the patient 
may lose all his teeth in a few months. It is very interest- 
ing to note that this may be connected with laryngeal crises, 
a fact which would indicate that there may be some truth 
in the view advanced by Buzzard (British Med. Journal, Feb- 
ruary 19, 1886), according to which the centre for bone nutri- 
tion lies quite close to that of the vagus. 

The so-called mal per for ant du pied (perforating ulcer), which 
begins with the formation of a bleb and leads to abscess forma- 
tion and necrosis of the tendinous and bony portions of the 
feet, is due to some trophic disturbance, and may become a 
source of great discomfort to the patient. 

Affections of the bones and joints, which are also of trophic 
origin, belong to the more frequent complications of tabes. 
The bones become extraordinarily brittle and fractures fre- 
quently occur without pain, and one could almost say without 



TABES DORSALIS. 



6n 



the knowledge of the patient. The seat of such fractures is 
most commonly in the femur, and, more especially in old 
women, in the neck of that bone. This remarkable fragility is 
of especial moment when it occurs, as it sometimes does, in the 
bones of the spinal column, and particularly in its lumbar por- 
tion, and gives rise to spondylolisthesis without it being pos- 
sible to decide whether or not the cartilages and ligaments 
were first affected and the disease of the bones was only sec- 
ondary (Kroenig, Zeitschr. f. klin. Med., 1888, xiv, 1, 2). 

Among the joint affections which are not essentially differ- 
ent from those produced by arthritis deformans, the " arthro- 





Fig. 167. Fig. 168. 

Fig 167. — Erosion of the Head of the Humerus in Tabes Dorsalis. Fig. 168.- 
Normal Humerus. (After Charcot.) 



pat/tie des ataxiques" or " Charcot's joint," because it was first 
described by him, deserves particular mention. According to 
his description, there develops in the course of one night, with- 
out any appreciable cause and without pain or febrile move- 
ment, a swelling of a joint — for instance, the knee, shoulder, 
elbow, or hip. In the course of a few days there is noted a 
collection of fluid in the joint and in the periarticular bursae, 
and on puncture a lemon-yellowish transparent serum can be 
withdrawn. In one or two weeks later one is able to make 
out more or less well-marked crepitation, due to changes in 
the joint surfaces. The joint becomes extraordinarily movable 
and luxations frequently occur, especially when the ends of 
the bone are worn away (Figs. 167 and 168). 

Occasionally the tarsus is affected by the process. In such 
cases a marked swelling of the foot occurs in a relatively short 



612 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 




Fig. 169.— Skeleton of a Tabetic Foot. (After Char- 
cot. ) (The original is in the pathological museum of 
Charcot's department in the Salpetriere in Paris.) 1-5, 
metatarsal bones. 6, internal cuneiform bone. 7, mid- 
dle cuneiform bone. 8, fragment of the external cunei- 
form bone. 9, cuboid bone. 10 and n, fragments of the 
scaphoid bone. 12 and 13, the astragalus. 14, the cs 
calcaneum. 



time, the joints be- 
come affected in the 
way stated above, 
and at the post-mor- 
tem examination the 
tarsal bones are 
found to be altered 
in the manner repre- 
sented in Fig. 169 
(" tabetic foot "). 

The real cause 
of the affection is 
not yet known. 
While Charcot con- 
sidered it due to an 
atrophy of the ante- 
rior ganglionic cells 
in the cord, Virchow 
pointed out that it 
might be due to a 
state of lowered nu- 
trition of the bone 
in consequence of 
nerve influence. Op- 
penheim and Siemer- 
ling demonstrated a 
degeneration in the 
peripheral nerves, 
and according to 
Volkmann the anal- 
gesia produced by 
tabes creates a pre- 
disposition to the oc- 
currence of the joint 
affection which he 
attributes to disturb- 
ances in the carti- 
lages. Rotter di- 
vides the cases in- 
to three groups — 
true arthritides de- 
formantes, primary 



TABES DOR SA LIS. 613 

fractures of the joints, and a third class in which there are most 
pronounced changes, but in which we are unable to determine 
whether they are due to an arthritis or a primary fracture. 

We may add tha\ arthrectomy has lately been performed 
several times for tabetic affections of the knee joint, and has 
been followed by success (Wolff, Sitzung der Berliner med. 
Gesellsch., 7. Marz, 1888, Deutsche med. Ztg., 1888, 22, page 
268). 

For the last few years only we have known that the periph- 
eral nerves play a large and important part in tabes; previous 
to this Tiirck and later Friedreich had reported alterations 
in the mixed nerves, but we were ignorant of their character 
until the publication of the work of Westphal (1878), which was 
soon followed by other articles, among them those of Dejerine, 
Pitres and Vaillard, Oppenheim and Siemerling, Sakaky and 
Pierret. The results of their work showed that the peripheral 
nerves suffer a parenchymatous degeneration, a destructive 
process, which, being associated with an increase of the peri- 
neurium, a proliferation of the nuclei, and extensive connective- 
tissue formation, leads to a final atrophy of the nerve elements. 
This peripheral neuritis is not necessarily followed by marked 
symptoms, but, according to our views, it is the main factor in 
the production of the analgesias which are often observed so 
early in the course of tabes, and to which O. Berger has already 
directed attention. Under certain circumstances this neuritis 
may produce deformities; thus if it involve the nerves which 
supply the muscles of the plantar surface of the foot these 
latter atrophy. The muscles concerned are those of the inner 
surface of the foot affecting the great toe, those of the outer 
surface to the little toe, the flexor brevis communis, and the 
interossei ; the plantar aponeurosis retracts, and the toes be- 
come flexed and immovable (Fig. 170). 

If larger nerves be affected by the process, the symptoms, 
w r hich are characteristic of neuritis, and which have been de- 
scribed on page 386, make their appearance. They are chiefly 
pains, motor disturbances, and muscular atrophies. To this 
class belong the musculo-spiral paralyses caused by tabes, de- 
scribed by Striimpell (Berl. klin. Wochenschr., 1886, xxiii, 37), 
lesions of the median, described by Remak (ibid., 1887, xxiv, 
26), and, lastly, lesions of the peroneus longus, as described by 
Joffroy (Gaz. hebdom., 1883, xxxii, 48). Lately Dejerine has 



614 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



described a widespread muscular atrophy in tabetics, which 
has its origin in a peripheral neuritis (Neurite motrice periphe- 
rique des ataxiques, Revue de med., 1889, 2). The observations 
of Remak seem to indicate that the muscles which are sub- 
jected to an unusual strain in the patient's occupation are par- 
ticularly prone to become atrophied. In confirmation of this 
I can add two cases of my. own : (1) In a cigar-maker, who ex- 
erted particularly the first three fingers of the right hand in 
making the cigar-tips, atrophy developed in the muscles of 




Fig. 170. — Plantar Flexion of the Toes in the Course of Tabes (personal ob- 
servation ). 



the ball of the thumb supplied by the median. (2) A dentist 
with tabes, who overexerted the musculature of the hand in 
filling teeth and in other manipulations, came under my obser- 
vation on account of an atrophy of the hypothenar muscles 
supplied by the ulnar. Similar cases are not uncommon. 

It is not at all rare in the course of tabes for the peripheral 
nerves to be attacked by neuralgias ; the sciatic nerve calls for 
first, mention, as it is usually affected early in the disease and 
very severely. We have already stated on page 370 that 
double sciatica is more particularly a frequent accompaniment 
of tabes. Branches of the pudic nerve may also be affected, 
and often recto-vesical neuralgia may be a source of great 
trouble (Neftel, Arch. f. Psych, und Nervenkrankheiten, 1880, 
10) ; in this the patients complain of a painful burning sensa- 
tion in the rectum after each defecation, which is often fol- 



TABES DOKSALIS. 



615 



lowed by marked depression of spirits, and the longer the in- 
terval between the acts of defecation and the firmer the con- 
sistence of the stool, the more intense becomes the suffering. 
After all, it is not easy to distinguish the peripheral from the 
above-described central affection, which may run a similar 
course. 

We will now attempt to say something as to the relative 
frequency of the symptoms and the time of their occurrence, 
but, of course, such statements can not lay claim to accuracy, 
and can only serve to give an approximate idea concerning the 
points in question. 

Among the most frequent symptoms belonging to the brain, 
are, as we have already shown, lesions of the cranial nerves, 
and particularly of the oculomotorius, by which transient diplo- 
pia and irregularities in the condition of the pupils (aniso- 
coria, myosis) are produced ; next come lesions of the abdu- 
cens. Almost as frequently will one recognize disturbances of 
the vagus, among which the gastric crises deserve particular 
mention. Among the spinal symptoms belonging to this cate- 
gory the first to be mentioned are the manifold disturbances of 
sensibility, among them cutaneous analgesias, particularly in 
the lower extremities, then, the parassthesias and the lancinat- 
ing pains which occur more particularly in the legs ; how far 
these symptoms in a given case are due to disease (irritation) 
of the posterior spinal roots or to lesions of the peripheral 
nerves can only be determined by microscopic examination. 
At all events, degeneration of the peripheral nerves in the 
most varied cutaneous areas is to be classed among the regu- 
lar occurrences in tabes. The disappearance of the patellar 
reflex and some form of the various bladder troubles are almost 
constant accompaniments of the affection, and these, taken in 
connection with the symptoms just mentioned, must be con- 
sidered as the foundation for the diagnosis. 

Lesions, particularly atrophy, of the optic nerve, symptoms 
of irritation and paralysis in the domain of the fifth nerve, and 
ataxia of the lower extremities, are frequent but less regular 
occurrences. 

Less frequently met with are the laryngeal crises, due to 
lesions of the vagus, and affections of the nerves of taste and 
of the accessorius ; the same may be said of the psychoses, 
hemiplegias, and attacks of epilepsy observed in the course of 



616 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

tabes. Certain disturbances of sensibility, the so-called rectal 
crises, cutaneous hyperesthesias, neuralgias of the peripheral 
spinal nerves, paraplegia of the legs, the tremor, and disturb- 
ances in the sexual functions also belong to this category. The 
trophic disturbances, the muscular atrophy, the falling out of 
the nails and hair, the " vial perforant du pied," and Charcot's 
disease of the joints are also comparatively rare. 

To the symptoms which occur only seldom, one might 
almost say exceptionally, belong those referable to the hypo- 
glossal, the auditory, and the facial nerves ; among the motor 
disturbances of spinal origin, the so-called associated move- 
ments and ataxia of the upper extremities, among the sensory 
disturbances, the so-called polysesthesias, double sensations, and 
delayed sensations belong to this class ; marked diminution in 
the muscular strength is also exceptional. 

As to the time at which these various symptoms severally 
arise, it is even more difficult to give reliable data, since there 
exists no uniformity; still one can state with some amount of 
certainty that next to a feeling of slight weariness, particularly 
in the legs, the lesions of the oculo-motor and abducens are 
often the first to make their appearance ; the disturbances of 
sensibility, particularly analgesia and paresthesia, as a rule 
also occur early, while lancinating pains make their appear- 
ance at a later period. The gastric crises are observed rela- 
tively early, and bladder troubles are among the more frequent 
occurrences before the disease has advanced very far. The 
disappearance of the patellar reflex, as it usually constitutes 
one of the initial symptoms of the disease, plays an important 
part in the diagnosis, as we have already shown. Pronounced 
motor disturbances, particularly ataxia of the lower extremi- 
ties, are often not observed until later in the disease, often only 
after years ; and paraplegia of the legs, when it occurs at all, 
characterizes the last stages of the disease. Optic atrophy 
sometimes makes its appearance relatively early ; in other in- 
stances it occurs only at a late period and comes on very grad- 
ually. For the time of its occurrence no definite rules can be 
laid down. Hemiplegias, epileptic attacks, and psychical dis- 
turbances, if they occur at all, manifest themselves sometimes 
earlier, sometimes later. As far as our own observations go, 
the trophic disturbances mentioned above, particularly the 
muscular atrophies and Charcot's joint affection, usually be- 
long to the later stages. 



TABES DORSALIS. 



6l 7 



The course of tabes is rarely markedly influenced by com- 
plications, and this will be readily understood when we con- 
sider that the affection presents such a manifold variety of 
symptoms, that it is almost impossible to add to it new ones, 
resulting from another and independent disease. On the other 
hand, one can readily imagine that a complication may exist 
and yet escape recognition. This would apply, for example, 
to hysteria, which may give rise to symptoms which, under 
certain circumstances, can not be distinguished at all from 
those of the disease under discussion. The same is true of 
syphilis, the nervous symptoms of which may be identical with 
those of tabes ; and, lastly, it may be applied to the progressive 
paralysis of the insane, as the manifestations of both diseases 
may be inextricably involved with each other. It is less diffi- 
cult in the case of diabetes, which has also been observed as a 
complication ; yet the diabetic and tabetic symptoms may com- 
pletely obscure each other, so that it becomes impossible to 
determine which are due to the one and which are due to the 
other affection. Should, however, the urine contain a large 
amount of sugar, the task becomes less complicated, for glyco- 
suria is not frequent in tabes. Moreover, as Mobius holds, the 
Argyll-Robertson pupil should make us decide for tabes, as it 
is absent in diabetes (cf. Fischer, Centralbl. f. Nervenheilk., 
1886, ix, 18). 

If we consider tabes as an affection of the entire nervous 
system, we shall not be surprised if now and again other lesions 
in the cord are found to be coincident with the tabetic process, 
as, for example, lesions in the crossed pyramidal tracts, which 
Eulenburg has observed and reported (Deutsche med. Wochen- 
schr., 1887, xiii, 35). The degeneration in the posterior col- 
umns, it is true, is the most common, but this would not ex- 
clude a simultaneous affection in other systems of fibres. 

Some German and French writers have assumed aortic in- 
sufficiency to be a frequent complication of tabes, but the work 
of Leyden (Centralbl. f. klin. Med., 1887, viii, 1) and his lucid 
statements at the session of the Verein fiir innere Medicin in 
Berlin on the 29th of October, 1888, have shown this connection 
to be a mere coincidence (Deutsche med. Zeitung, 1888-89). 

Course. — About the general course of the disease the fol- 
lowing remarks will hold good in a large number of cases: A 
middle-aged person who has become infected with syphilis 
some years previously, usually from eight to fifteen years be- 



6i8 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

fore, begins to complain of slight fatigue on walking and occa- 
sional pains in the lower extremities. In spite of all treatment 
the pains continue to be troublesome, and occasionally become 
so severe that they disturb the patient's rest at night or even 
render sleep impossible. At the same time it appears to him 
that his vision is becoming affected, and he complains particu- 
larly that he sees double, and in consequence suffers from ver- 
tigo. The diplopia may last only for a few moments at a time. 
The vertigo, which at the onset of the trouble was insignifi- 
cant, beco.mes more and more pronounced, more especially in 
the dark, so much so that it is almost impossible for the patient 
to pass through a dark room without help. He also discovers 
that he staggers or falls to one side in the morning when in 
washing he covers his face with the towel, and only regains his 
equilibrium when his eyes are free again. Finally, he complains 
that he is obliged to pass water more often than usual, and that 
he consumes more time and must exert himself more when 
urinating than previously. The objective examination shows 
that there is widespread anaesthesia, particularly analgesic 
areas, about the lower extremities, and a loss of the patellar re- 
flex. He may be inconvenienced in this way for years with- 
out his condition becoming serious. He suffers more or less 
all the time, sometimes quite severely, but, on the whole, his 
existence is quite bearable. The state of his mind is hopeful, 
for the daily occupation has not yet been interfered with by 
the disease. 

The aspect of affairs is quite different when the patient suf- 
fers from gastric disturbances. The appetite becomes poor, 
and occasionally — sometimes for weeks at a time — there is morn- 
ing vomiting, which is quite profuse and occurs as soon as the 
patient awakes, when, without effort, watery, slimy masses are 
discharged. After lasting for a longer or shorter time this 
ceases, probably only to return later on. The appearance of 
the patient, which was previously natural, now becomes al- 
tered for the worse. The skin becomes yellow and wrinkled, 
and his friends and acquaintances, who have not seen him for 
some time, begin to inquire about his health. At the same time 
a new symptom makes its appearance, and he notices that his 
gait is becoming uncertain and that in walking he must invoke 
his eyes to aid his legs, which, instead of carrying out the 
movements he intends, are thrown out in a peculiar aimless 
manner, so that if he be not led or supported he runs the risk of 



TABES DOR SA LIS, 619 

tumbling down. This trouble in walking, which is associated, 
perhaps, with occasional gastric and more rarely with laryngeal 
crises, may likewise continue for years ; but if the ataxia impli- 
cate the upper extremities, as happens in a small proportion of 
the cases, it may so interfere with the patient's occupation that 
he may be unable to continue it. In the meanwhile the blad- 
der symptoms become more prominent and are aggravated to 
such an extent that it becomes necessary for the patient to 
wear some sort of receptacle, while the marked contraction or 
inequality of the pupils is apparent even to the layman. 

Gradually another change for the worse in the gait comes 
on. The legs, which, although thrown out in the characteristic 
manner, in other respects performed their duty and even en- 
abled the patient to cover considerable distances, begin to be 
fatigued on the slightest exertion ; they become heavier and 
heavier, and it becomes more and more difficult, and at last 
needs the greatest effort, to walk at all. The legs are so weak 
that they are no longer able to support their owner, who is 
forced to take to the invalid's chair, and in this he ends an 
existence, the last years of which are as wretched as could be 
imagined, especially if atrophy of the optic nerve has robbed 
him of sight and the lancinating pains make his days and nights 
miserable. When the disease progresses in this or a similar 
manner its duration varies from ten, fifteen, even to twenty 
years or more. It can, however, be considerably shorter. I 
have seen cases in which only from three to five months 
elapsed between the beginning of the affection, from the first 
appearance of the disturbances in the movements of converg- 
ence of the eyes, to the appearance of well-marked paralysis 
of the legs. 

On the other hand, there are cases in which the course may 
extend over a space of thirty or more years ; in these cases 
paralytic symptoms may not come on at all, and the ataxia con- 
tinue to the end. There are tabetics who during their entire 
illness are hardly prevented at all from carrying on their 
work ; they are always able to be up and about, and it appears 
as if the different symptoms never attained their full develop- 
ment in these cases. These are the so-called "formes frustcs" 
of the French, analogous to those with which we have already 
become acquainted in Graves' disease and in multiple sclerosis. 
Again, in other cases, tabes sets in with brusque symptoms, 
such as apoplectiform attacks, disturbances of speech, and 



620 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

lesions of the optic nerve, and then pursues a mild course for 
a long period — violent symptoms, such as laryngeal crises, in- 
tense neuralgias, etc., only occurring occasionally ; these are 
the so-called atypical forms of the authors. 

From what has been said it is evident how difficult it is to 
make a positive statement concerning the general course of the 
affection. Scarcely one case follows the same course as an- 
other, and it often requires a great amount of caution and ex- 
perience to enable one to take a correct view of all that oc- 
curs. 

Just as much uncertainty exists about the prognosis, which 
is influenced by various factors. One most important question 
is, of how long standing is the disease, for in recent cases in 
which there are no other symptoms than disturbances of sen- 
sibility and absence of the knee jerks, and the course of which 
has not as yet exceeded three or four months, and in which 
there is no ataxia, the prognosis is not at all unfavorable, and 
the disease is under some conditions curable. Advanced cases 
of tabes in which there are numerous spinal and cerebral symp- 
toms offer a much more serious prognosis, but even here the 
possibility of cure is not excluded, though the highest percent- 
age of recoveries is estimated at one per cent (Eulenburg). Of 
course, one can not expect that the anatomical changes will 
disappear, and at the autopsy a widespread degeneration of 
the posterior columns has been found in cases in which during 
life all symptoms had practically disappeared. In the majority 
of the so-called recoveries from tabes one is led to believe that 
there was a mistake in the diagnosis, and that these were cases 
of chronic nicotine poisoning, peripheral neuritis, hysteria, 
neurasthenia, etc. The prognosis of old cases with paraplegia 
of the legs, paralysis of the bladder, and so forth, is altogether 
unfavorable, and any attempts at cure are not only useless, but 
may even interfere with the comfort of the patient. 

It is a matter of indifference, so far as the prognosis is con- 
cerned, whether one is able to demonstrate that the patient has 
at one time or other been infected with syphilis or not ; a so- 
called specific or luetic tabes, especially when the infection has 
taken place ten or twenty years previously, does not afford a 
better outlook than the more rare idiopathic affection. 

It is clear, then, that one must be very cautious in predict- 
ing the duration of the disease ; one can not say definitely how 
many years a tabetic patient has to live, and just as little should 



TABES DORSALIS. 6 2I 

one attempt to make a positive statement as to how long the 
patient will be able to work. The condition may remain quite 
endurable for months or even years, and the outlook may ap- 
pear quite hopeful, particularly in regard to the capacity for 
work, and yet suddenly a marked change may take place; pro- 
nounced ataxia, cerebral symptoms, or the like may manifest 
themselves, which render the patient incapable of following 
any occupation. The more cases one sees, the more cautious 
does one become in giving a prognosis, and the more distrust- 
ful of the reports of so-called cures — at least when old cases 
are concerned. 

Diagnosis. — As one can readily see from what has been 
said, the diagnosis of tabes is sometimes one of the simplest 
possible tasks for the physician ; in other instances it can not 
be made with certainty for a long time. Thus it may under 
certain circumstances be very difficult to differentiate between 
the disease under consideration and complicated cases of syph- 
ilis of the brain and spinal cord, diabetes, or hysteria. It seems 
perfectly possible for one to consider a severe case of neuras- 
thenia for a long time as one of tabes, but the further course 
and final success of therapeutic measures will demonstrate the 
error. When in the course of tabes the sensory and bladder 
disturbances are only slightly marked, there may be question 
of the existence of a chronic anterior poliomyelitis, but usually 
the lancinating pains, the paresthesias, the affection of the eye 
muscles, and the mere fact that bladder symptoms exist at all, 
afford sufficient grounds on which to base a diagnosis. In dis- 
eases of the vertebral column, in the course of which lancinat- 
ing pains, " Westphal's sign," and bladder symptoms may be 
found, an examination will reveal that the vertebral column 
itself is affected, and the spinous processes are painful on press- 
ure — a condition which is sufficient to settle the diagnosis. 
The mistake of considering a tabophobe, or a person who im- 
agines he has tabes, as a real tabetic, can only occur when a 
careful examination is neglected, and the physician is afraid to 
adopt any energetic, psychical as well as somatic, treatment. 
As soon as this is instituted the tabetic symptoms will turn out 
to be mere hypochondriacal notions, and recovery will quickly 
follow. 

It is of practical importance to note that the various symp- 
toms occurring in tabes are also observed in other affections. 
In these cases there is much room for errors in diagnosis, the 



622 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

most important of which we wish to bring to the reader's at- 
tention. 

Paralysis of the eye muscles and pupillary symptoms are, 
as we have remarked, very common in the course of tabes. 
Another affection in which they also occur is multiple sclerosis. 
Here, however, diplopia as well as strabismus are rare, while, 
on the other hand, nystagmus is very frequent, and the pupil- 
lary reaction to light is preserved. Myosis occurs in this affec- 
tion as well as in tabes, but whereas in the former the pupils 
contract still more under the influence of light, in tabes they 
usually remain immobile under the same circumstances. 

Symptoms referable to the optic nerve — amblyopia, for in- 
stance — are also observed as the effect of different poisons 
(page 37). In such cases the history will be of great assist- 
ance to us in making the diagnosis. Amblyopia developing in 
the course of multiple sclerosis is not accompanied, as in tabes, 
by a contraction of the field of vision, nor does it steadily grow 
worse ; but remissions occur, and the improvement may even 
last for a considerable time. It has already been shown on 
page 580 that the optic atrophy of multiple sclerosis differs in 
important points from that occurring in tabes. It should also 
be remembered that there is an optic atrophy in which the 
morbid process is confined to the optic nerve, and in which it 
is impossible to demonstrate any general nervous disease. 

The various visceral " crises," in which tabes abounds, can 
likewise be produced by independent affections of the vagus. 
Here one must rely upon the more characteristic symptoms of 
tabes, particularly Westphal's and Romberg's signs. That 
"gastric crises" alone can not enable one to make the diagno- 
sis is all the more to be insisted upon since Debove has recently 
observed them in neurasthenics (Soc. des hop., seance 1888, 
xii, 28). 

The motor disturbances which we find here, and of which 
the most important is the ataxia of the lower extremities, ap- 
pear not only in the course of tabes, but also in other diseases 
in which one is unable sometimes to ascertain their anatomical 
basis. This is more especially true of the so-called functional 
ataxias (Gallard, Jaccoud), which develop sometimes with, 
sometimes without sensory disturbances, and are associated 
with no other symptoms. Ataxia has likewise been observed 
developing slowly or quickly after diphtheria (Berl. klin. 
Wochenschr., 1887, 49, p. 930), after quickly succeeding preg- 



TABES DORSALIS. 



623 



nancies, and in the course of diabetes ; and the question must 
remain undecided whether it is to be considered as the expres- 
sion of a severe general affection, of a faulty composition of 
the blood and an imperfect innervation dependent upon it, or 
as the result of a peripheral neuritis developing under the 
influence of an infectious agent. However, it can not be diffi- 
cult in a given case to determine whether the ataxia is to be 
regarded as of spinal or tabetic, or as of functional or of in- 
fectious origin. 

The lancinating pains also occur in affections of the verte- 
bral column, e. g., in Pott's disease, when the posterior roots 
are irritated, but the deformity and the tenderness of the ver- 
tebras upon pressure will make the diagnosis clear. 

Other pains, following the course of various larger nerves, 
which can last for weeks or months without marked exacerba- 
tions, and be accompanied by paresthesias, formication, numb- 
ness, etc., are observed not only in tabes, but also in peripheral 
neuritis, following, for example, the abuse of alcohol. If to 
these a temporary loss of the patellar reflex be added, we have 
the picture of what is called pseudo-tabes, and a cautious and 
often-repeated examination is necessary in order to make the 
differential diagnosis. The history and the further course of 
the disease, which in alcoholic neuritis may become favorable 
after the removal of the cause, should always be taken into 
consideration. 

We have already pointed out on page 606 the circumstances 
under which Westphal's sign may be present, and we can not 
insist too strongly that it is an error, or at least a too hasty 
conclusion, to think only of tabes whenever the patellar reflex 
is absent. On the other hand, we must not imagine that its 
presence puts tabes out of the question, for the possibility of 
the existence of this disease is not at all excluded when the re- 
flex is found to be normal. 

Pathological Anatomy. — Considered from the pathological 
standpoint, tabes represents a degenerative process in which 
the entire nervous system takes part. The reason that we are 
unable in all cases to demonstrate the participation of all the 
nerves — that in many cases, for example, the cord seems to be 
the part most involved while the brain and its nerves appear 
less affected — lies in the fact that we have been accustomed to 
examine the cord with the greatest accuracy, while the brain 
and peripheral nerves were only considered of secondary im- 



624 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

portance ; and, secondly, in the fact that many cases are ter- 
minated by intercurrent diseases before the degenerative proc- 
ess could develop in all directions. 

This degeneration, which consists principally in the death 
of the nerve elements and an increase of the connective tissue, 
presupposes a certain change in the nervous system, the nature 
of which we do not as yet know, and which is peculiar to the 
individual either as the result of hereditary influences or which 
has been acquired later through syphilitic infection. The con- 
genital predisposition is not sufficient to produce an outbreak 
of the disease. For this some one of certain exciting causes, 
of which we shall speak later, is needed. On the other hand, 
the changes produced in the nervous system by a syphilitic 
infection are able of themselves to lead to the production of 
tabes. As to the manner in which heredity works in the pro- 
duction of these changes, we are not in a position evqn to haz- 
ard a conjecture, nor are we by any means certain of the pre- 
cise mode of action of syphilis. In this latter case, however, 
it is, according to our idea, most probable that the changes are 
the result of a syphilitic affection of the blood-vessels. It is, in 
our opinion, less likely that a poison (" toxine "), which affects 
the nervous system, is developed secondarily, in which case 
tabes would have to be regarded as a post-syphilitic affection, 
just as paralysis of the soft palate is a post-diphtheritic affec- 
tion (Strumpell) ; and it would be still harder to imagine that 
the syphilitic virus becomes localized in the nervous system, 
and, as such, later produces the disease (Rumpf). One could in 
the last case not help but ask how it is possible for ten, fifteen, 
or more years to elapse between the syphilitic infection and 
the appearance of the first tabetic symptoms, a circumstance 
which, on the other hand, could be easily explained by assum- 
ing the existence of anatomical changes which are due to a 
diminution in the blood supply and require a relatively long 
time for their development. 

The degeneration begins probably always in the peripheral 
nerves. The terminations of the cutaneous sensory nerves may 
be the first to become affected. The admirable researches of 
Dejerine, Oppenheim, Siemerling, and others, have clearly 
demonstrated the participation of the peripheral nerves in the 
tabetic process, and there is no doubt but that they appear just 
as much degenerated as the posterior roots, in which the atro- 
phy was shown to be most marked between the spinal ganglia 



TABES DOR SALTS. 



62$ 



and the cord, while the peripheral portion was often relatively 
quite free (Dejerine, Compt. rend, de la Soc. de biol, 1882, page 
215). The degree to which the several cutaneous nerves are 
attacked varies. Those of the legs are usually more affected 
than those of the upper extremities. No definite rule can be 
said to exist. Sometimes, and this often happens, the periph- 
eral ends of certain of the cranial nerves are the first to be- 
come diseased — e. g., those of the optic, the oculo-motor, and 
the abducens — and then the symptoms described above appear 
in the initial stage. At any rate, the first symptoms develop 
in consequence of lesions of peripheral end organs. 

The degenerative process in the cord, which occurs later, 
is the most prominent pathological feature at the autopsy, and 
formerly was considered the only, or at least the only charac- 
teristic lesion. This explains why tabes was and is still con- 
sidered, by the majority of authors, as a disease of the spinal 
cord. According to our idea this is not true. It is rather an 
affection of the entire nervous system, in which the cord is 
not even the first part to become affected, but later is altered 
in such a characteristic and striking manner that we can not 
be surprised if the other, less marked, conditions were over- 
looked. Though the changes in the cord have long been rec- 
ognized, the views as to their origin are still conflicting and 
the most varied interpretations have been put forward. We 
do not care to enter into an account of the controversies, but 
will only bring before our readers succinctly the conclusions 
arrived at as to the nature of the affection. It consists prob- 
ably of a primary degenerative atrophy of the nerve fibres, 
which is followed by a secondary increase of the connective 
tissue. As the degeneration takes place slowly, few compound 
granular corpuscles are found, and only in older cases can cor- 
pora amylacea be demonstrated. The grayish discoloration of 
the posterior columns depends upon the destruction of the 
medullary sheaths. A marked degree of atrophy is to be no- 
ticed in the posterior columns, and in advanced cases the 
entire cord appears narrower and thinner than is normal. 
On cross section it is readily demonstrable that besides the 
posterior columns the posterior gray horns and the posterior 
roots also become atrophied. Moreover, it is of interest to 
note that certain portions of the cord seem, as a rule, to be 
spared, while others are almost always involved in the degen- 
eration which affects both sides of the cord symmetrically. 
40 



626 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

The lesion is of the character which we have learned to recog- 
nize in the so-called " combined system diseases " — that is, cer- 
tain systems of fibres which have certain anatomical and 
physiological relations to one another become diseased, while 
others are unaffected. It is also seen that not all portions of 
the posterior columns are implicated equally (Striimpell), but 
that the extent of the lesion differs according to its situation. 
For example, it is most severe in the lumbar region, in which 
only the anterior part is left intact, the middle and posterior 
portions being degenerated. In the cer- 
vical region there are to be distinguished 
four fields on either side, of which, two, 
Goll's columns and a part of Burdach's 
columns, the so-called lateral root fields 
(into which direct fibres enter from the 
Fig. 171. posterior nerve roots), appear degener- 





Fig. 172. Fig. 173. 

Fig. 171. — Section through the Cervical Cord in a Case of Commencing Tabes. 
Fig. 172.— Section through the Lumbar Cord in Tabes. Fig. 173.— Section 
through the Cervical Cord in a Case of Advanced Tabes. (After Strum- 
pell.) 

ated, while two others, one anterior and lateral, the other 
posterior and external (the posterior outer fields of Striim- 
pell), appear normal (Figs. 171, 172, and 173). Such a dis- 
tribution of the lesion is frequently observed, but naturally 
not found in all cases. We have already mentioned that the 
posterior gray matter is involved in the process. Lissauer 
deserves credit for having demonstrated (Arch. f. Psych, 
und Nervenkrankheiten, 1886, xvii, page 376) that here the 
affection of the fibres in Clarke's columns should be distin- 
guished from that of the fine and large root fibres in the 
posterior horns. Physiologically, this discovery can not as 
yet be utilized. 

Of the lesions in the medulla oblongata and the brain, pro- 



TABES DORSALIS. 



627 



duced by tabes, the former affect the cranial nerves at their 
nuclei or in their peripheral course. Of the manifold symp- 
toms produced thereby we have spoken before. On the other 
hand, we may have lesions of the cortex, an implication of 
which in many cases can not be called into question. We also 
said that some of the nuclei, particularly those of the eye mus- 
cles, of the vagus, and of the hypoglossus, are affected more 
often and more severely than others, while, for instance, the 
facial, the auditory, and the glossopharyngeal remain as a rule 
intact, a fact for which we have no explanation. According to 
Jendrassik's conception (Deutsches Arch. f. klin. Med., 1888, 
xliii, 6), the brain is the primary seat of the tabetic process, so 
that the sensory disturbances and the ataxia are to be consid- 
ered as of cortical origin, and the degeneration in the posterior 
columns, and perhaps those of the direct cerebellar tracts, as 
secondary processes. Until the cortex has been examined 
microscopically in the initial stages of the affection, and some 
constant changes have been demonstrated in it after death, this 
theory, like all the others, will remain nothing more than a 
bare hypothesis, and can be neither contradicted nor yet 
accepted. Such a pathogenesis, however, is not impossible, 
though it is not difficult to bring forward objections to it. 

Lastly, it should be mentioned that Basso (Ann. univers. di 
med. et chir., June, 1886) considers tabes to be an affection of 
the sympathetic system, under the influence of which the cere- 
brospinal lesions develop. He thinks that the anatomical 
changes in the nervous system are at first caused by functional, 
and later by organic disease of the blood-vessels, and holds 
that when taken in time tabes is curable. 

^Etiology. — In speaking of the aetiology of tabes, one must 
constantly distinguish, as is evident from the views expressed 
above, between the non-syphilitic and the syphilitic affection. 
In the first case one should above all take into consideration 
the hereditary conditions in order to comprehend the congen- 
ital predisposition which is necessary for the production of the 
disease. By this we do not mean to class tabes among the 
hereditary diseases in the ordinary sense of the word, for it 
certainly can not come under this category ; on the contrary, 
we are justified in assuming that direct inheritance of it is 
quite rare. By heredity in this connection we mean a general 
neuropathic inherited tendency, or, in other words, that in the 
family of the patient all kinds of neuroses, not excluding psy- 



628 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

choses, have occurred repeatedly. Not only the parents, but 
also more distant relatives, e. g., aunts, uncles, or grandparents, 
may have suffered with progressive paralysis of the insane, 
epilepsy, melancholia, hysteria, migraine, etc., and it is just this 
heredity which in the presence of exciting causes is sufficient 
to open the door to the tabetic process. The labors of Charcot 
(Arch, gener. de med., September, 1883) an d the comprehensive 
statistics of Ballet and Landouzy (Arch, de neurol., 1886, vii, 
20) have thrown an interesting light upon this subject, and 
have brilliantly substantiated the view which Trousseau ex- 
pressed at an earlier period, that tabes was (in the sense of the 
word as expressed above) hereditary. Among the German 
authors Mobius has occupied himself particularly with this 
subject (Allg. Zeitschr. f. Psych., 1883, xl, 1, 2). 

The exciting causes which relatively frequently lead to the 
development of tabes (in those with hereditary tendencies) con- 
sist (a) in exposure to cold and wet, to sudden changes of tem- 
perature, and to prolonged living in damp lodgings ; (&) in 
traumatic influences ; (c) in certain factors due to the daily oc- 
cupation, the most important of which is overexertion. The 
opinion that sexual excesses may lead to tabes, which has been 
expressed by various authors, must be given up as without 
proof. 

I have never questioned but that exposure to cold, sudden 
changes of temperature, and, particularly, severe wettings, may 
play an important part in the aetiology of the affection ; still, to 
me the following case was particularly convincing: The pa- 
tient, a general agent for several hail-insurance companies, fifty- 
eight years old, had had syphilis thirty-nine years before, since 
which time he had been perfectly well. In August, 1885, while 
estimating the damage caused by a hailstorm, he was drenched 
to the skin, and was obliged to spend several hours in his wet 
boots. Three months later the first tabetic symptoms made 
their appearance — parassthesia and anaesthesia of the legs, loss 
of the patellar reflexes, etc. ; by Christmas, 1885, he was mark- 
edly ataxic, and in the spring of 1886 he was unable to pursue 
his calling. In the summer of 1886 he suffered with intestinal 
crises and intense lancinating pains, and eighteen months from 
the beginning of the affection he had paraplegia of both legs. 
In the early part of 1887 he died from an intercurrent attack 
of pneumonia. When tabes develops in one well on in the fif- 
ties, there must be some particular cause for it, and in this case 



TABES DORSALIS. 629 

it was, without doubt, the wetting. Similar cases can easily be 
found if the history be carefully taken. 

The role which traumatic influences play in the production 
of the affection is just as certain. In one of my cases, a gov- 
ernment official of high position, who had been affected with 
syphilis twenty-nine years before, met with an accident on a 
glacier in the summer of 1884. He fell and slid some distance 
on a snow field with great rapidity, but no bones were broken 
and no dislocation occurred. A few months later the first 
tabetic symptoms made their appearance, and now the disease 
is well developed. Again, a fall from a height may be the 
cause (Oppenheim) ; Strauss reports numerous traumatic cases 
(Faits pour servir a. l'etude des rapports du traumatisme avec 
le tabes. Arch, de phys., November, 1886). From his com- 
munication it is apparent (1) that years may elapse after the 
accident before the disease makes its appearance, and (2) that 
the traumatism may have an influence in determining the seat 
of the early symptoms, particularly of the lancinating pains, so 
that, for example, after a fracture of the lower part of the left 
leg the pains will first make their appearance at that point, and 
so forth. In an article by Spillman and Parisot (Traumatisme 
peripherique et tabes, Revue de med., 1888, 3) there is a table 
which gives the different forms of injury which have been 
followed by tabes. 

I have already pointed out, in my book on diseases of the 
laboring classes, that the occupation is not without importance, 
and more especially overexertion — for instance, at the sewing 
machine — and hard bodily labor in general, may be the cause 
of the outbreak of the disease in those who are predisposed to 
it. However, the percentage of such cases is not large. Hof- 
mann gives an instance which may be classed partly with those 
cases in which the occupation, partly with those in which trau- 
matism is the exciting cause. The patient was a laborer en- 
gaged in cutting tin plates, and in the course of his work his 
body was shaken from six to ten thousand times daily ; under 
the influence of these shocks the disease developed (Arch. f. 
Psych, und Nervenkrankheiten, 1888, xviii, 2, 439). 

Concerning the syphilitic tabes, which has been studied 
with the greatest care by Fournier and Erb, it is an undoubted 
fact that syphilis by itself is usually a sufficient cause for the 
disease, and that no other exciting factor is needed for its de- 
velopment. 



630 DISEASES OE THE GENERAL NERVOUS SYSTEM. 

We do not know what percentage of persons who have had 
syphilis become tabetic, but we do know for certain that the 
great majority of tabetics have had syphilis at some time or 
other — according to Erb, sixty per cent; according to Fournier, 
ninety per cent. Syphilis is more frequently followed by tabes 
than hereditary and exciting causes put together. Out of two 
hundred and forty-seven cases of tabes which I have seen in 
the last few years of my practice, in twenty-nine a syphilitic 
history was not obtained, while in the other two hundred and 
eighteen cases it was demonstrated with certainty, so that my 
figures almost correspond with the ninety per cent of Four- 
nier. Minor points out in his statistics (Wyestnik psychiatri 
i nervipatologii, 1888, vi) that tabes is much rarer in Russia 
among the Jews than among the other Russians, which is 
simply due to the fact that the former are less frequently 
syphilitic. The communication of Nagel also deserves con- 
sideration. He found in 1403 cases of tabes forty-six per cent 
of syphilitics, and out of 1450 other patients only nine and one 
half per cent. The time which elapses between the infection 
and the first appearance of tabes varies from a few months to 
one, two, five, fifteen years or more. The severity of the 
syphilis does not appear to stand in any relation to the severity 
of the tabes ; for one can observe very pronounced tabetic 
symptoms after an apparently trivial and quickly healed pri- 
mary sore, whereas sometimes after the most severe form of 
syphilis the general affection of the nervous system only ap- 
pears in its mildest form. 

The influence which age and sex exert in the production of 
the disease can only be considered in the non-specific cases. 
It is, however, only of slight importance ; for, although it is 
true that males are far more frequently affected than females 
(the proportion being seven to two), and although most of the 
patients are middle-aged, these facts can very well be accounted 
for by the nature of the several exciting causes, which make 
it comprehensible why men in the prime of life furnish rela- 
tively the greatest contingent of cases. 

Lastly, it must be confessed that in a few cases, which, 
however, form an exceedingly small fraction of the whole num- 
ber, no serological factor can be made out — neither hereditary 
predisposition, nor exciting causes, nor syphilitic infection. At 
present we can only acknowledge our ignorance of their patho- 
genesis. 



TABES DORSALIS. 63 1 

Prognosis. — From what has been said, we may infer what 
the prognosis will be. Though it is not absolutely unfavorable 
quoad vitam, inasmuch as the patient may linger on for years, 
and sometimes tens of years, one should not forget that in 
general the course is unfavorable, that the patient will suffer 
greatly at times, and that the final lot of the tabetic is almost 
always a total inability to work or gain a living. In discuss- 
ing the prognosis as to complete recovery, the question arises, 
Is tabes ever curable, or is there even a possibility of cure? 
This question is, with the proper restrictions, to be answered 
in the affirmative ; it is possible to cure tabes, but only fresh 
cases of luetic origin. Advanced cases, in which degeneration 
in the cord has taken place, are incurable ; we possess no means 
of bringing the lesion to a standstill or causing it to disappear. 
It is evident that the chances for the successful treatment of 
recent cases are increased the younger the patient and the 
better his general constitution. The prognosis is, ceteris pari- 
bus, less favorable in individuals with a neuropathic tendency, 
in whom the disease breaks out in consequence of some ex- 
citing cause, than in fresh specific cases. On the whole, one 
can say that out of two hundred and fifty tabetics one has a 
chance of regaining his previous health. 

Treatment. — In taking charge of a case of tabes we must 
first see that we ourselves, as well as the patient, clearly under- 
stand how much can be expected from any treatment. If his 
is one of those exceptional cases in which the prognosis is 
relatively favorable, we may tell him so ; but in most instances 
it will be our painful duty to make him acquainted with the 
seriousness of the situation, of which he will often be entirely 
ignorant. We must tell him with gentleness that a complete 
recovery can not be hoped for, and that all that it is possible to 
accomplish is to relieve some of his symptoms and to keep him 
in such a condition that he can as long as possible carry on his 
occupation. There is no disease in which it is more out of 
place to arouse in the patient vain hopes of recovery than in 
tabes. 

The choice of the therapeutic measures themselves depends 
upon the stage of the disease in which we find the patient — 
that is, upon how long he has been sick. In old cases the 
greatest caution ought to be observed, and one should not 
forget that rash therapeutic interference may do more harm 
to the patient than good. The value of a treatment is often 



632 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

quite problematical ; its harmfulness is too often quite evident. 
Hygienic and dietetic measures, conscientious nursing- and 
cleanliness, injections of morphine in severe attacks of pain, 
occasional cool baths, ever-repeated kindly encouragement, 
these constitute — if we leave out the suspension method, of 
which we shall speak later — the only treatment which old cases 
of tabes need, or, for that matter, can stand. But the recent 
cases also demand a great deal of care and forethought. In 
view of the duration of the treatment, protracted as it will 
probably be, all circumstances have to be taken into account — 
the constitution, the age, the occupation, and, above all, the 
pecuniary situation of the patient. 

As syphilis is at the bottom of so many instances of tabes, 
the question whether we are justified in expecting anything 
from an antisyphilitic treatment should be mooted, but only in 
exceptional cases can we have such a hope — that is, only when 
either signs of syphilis are still present, or when the time that 
has elapsed since their disappearance is relatively short (not 
longer than a few months or at most a year). Such cases are 
very rare ; generally years, perhaps twenty years, will have 
gone by during which the patient has been apparently per- 
fectly well, and then the antisyphilitic treatment is of no avail. 
If, however, we wish to institute it for any reason, possibly be- 
cause the patient himself insists upon it, bold doses ought to 
be given, four, six, even eight grammes (3j-3ij) of potassium 
iodide a day, and from three to six grammes (grs. xlv-3jss.) of 
mercurial ointment rubbed in daily. In all, two or three hun- 
dred grammes ( § vj— 5 i x ) of potassium iodide and the same 
amount of mercurial ointment ought to be used. 

If we have resolved to try internal medicines, knowing, of 
course, that there is none which acts favorably upon the dis- 
eased nerve elements, we may begin with silver nitrate in doses 
of one centigramme (gr. l / 7 ) in pill form three times a day for 
four or six weeks, after which time it may be combined with 
ergotin (arg. nitr., 0.3 (grs. ivss.) ; extr. secal. corn., 3, (grs. xlv) ; 
pulv. et extr. quass., q. s. ut f. pil. no. 30), of which also one 
pill is to be taken three times a day. Finally, a trial may be 
made with the salicylate of physostigmine, of which one milli- 
gramme (gr. J / 66 ) in pill form may be given three times a day 
for a month, as recommended by Meyer in his paper on the 
Influence of Physostigmine upon the Patellar Reflex (Berlin, 
klin. Wochenschr., 1888, 2). With these drugs we may be fairly 



TABES DORSALIS. 



633 



confident that we are doing- no harm, and often we may per- 
ceive a distinct improvement in the condition of the patient, 
although we are, of course, not able to definitely decide whether 
this is actually to be attributed to the medicine or not. We 
would recommend these remedies more warmly than any other, 
even than strychnine, which has been administered subcutane- 
ously in doses of from three to five milligrammes (gr. % 2 -/ 13 ), 
gradually increased to one centigramme (gr. */ 7 ) in twenty-four 
hours, for repeatedly after these injections we have observed 
the occurrence of pains, which had not been present for months. 
In the treatment of the individual symptoms we must resort to 
the same measures that we should adopt when these appear in 
the course of other diseases or by themselves ; for instance, for 
the lancinating pains, as in other neuralgias, we shall be obliged 
to give antipyrine and antifebrine, which have recently been 
recommended by Lepine, Suckling, Germain See, G. Fischer, 
and others, but we shall be driven to the conclusion finally, 
that for the relief of these pains there exists only one drug by 
the help of which the patient's painful existence may be ren- 
dered at all bearable — viz., morphine, which here more than 
in any other disease we are justified in using in large amounts. 
Gastric and laryngeal crises, headache, etc., are to be treated 
symptomatically. 

In addition to the internal medication, it is especially the 
electrical treatment which deserves consideration, This, if 
used at a period early enough, may be followed by excellent 
results, and may alone sometimes be capable of effecting a cure 
or an arrest of the morbid process. On the other hand, if we 
do not select our cases properly — for example, if we treat old 
cases like recent ones — we may do more harm than good with 
it. It may give rise to severe pains, and make the patients, 
who until they were treated by electricity were in a fair con- 
dition, begin to suffer terribly and soon lose confidence in the 
physician. Electricity may also prove successful against the 
motor disturbances, not so much against the ataxia as against 
the weakness in the legs ; also in combating anaesthesias and 
paresthesias in the hands and feet it may have some effect, 
whereas it is usually of little avail against the lancinating and 
rheumatoid pains. How to use the electricity, whether in the 
form of the faradic or the galvanic current, it is impossible to 
say in a few words. Every one forms for himself, in the course 
of years of practice, his own technique, and gives preference 



634 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

to this or that method ; the one prefers the galvanic, another 
the faradic ; again one will recommend the ascending, another 
the descending current through the spinal cord ; the one be- 
lieves in moist, the other in dry electrodes, especially the brush. 
Among all the different methods, besides the excellent general 
faradization advised by Beard and Rockwell, the faradic brush 
applied to the back, as recommended by Rumpf, has perhaps 
met with a more favorable reception than any other practice, 
and justly so. We prefer it, as far as electrical treatment goes, 
to all other modes. Details on the subject may be found in 
Erb's Handbuch der Elektrotherapie (Leipzic, Vogel). The 
treatment with dry cups, which has been urged by Lymann 
(Journ. of Nerv. and Ment. Diseases, July, 1887, xiv, page 409), 
is said to exert a favorable influence upon the nutrition of the 
muscles and the cutaneous nerves, by the rarefaction of the air, 
and thus to diminish the sensory disturbances. In recent cases 
this method may be made use of with good results. 

In a large number of cases the cold-water treatment was 
found to be extremely beneficial. The action of the water on 
the peripheral nerve endings, the influence which cold douches, 
wet packs, moist (" Priessnitz's ") abdominal bandages, cool 
baths, etc., exert upon the circulation in the vessels of the skin, 
and thus upon the terminal nerve twigs, is often so favorable 
that marked improvement during and after a stay in a hydro- 
therapeutic establishment is not rarely seen. Even in cases in 
which sensory and motor disturbances have attained to such a 
degree that but little can be hoped for, a carefully conducted 
cold-water treatment may be quite beneficial in improving the 
general condition of the patient and raising his spirits. 

On the other hand, we would emphatically warn against 
the use of warm or hot as well as steam and sweat baths. As 
a rule they are of no avail, but often evoke the lancinating 
pains. Unfortunately, the physician is not always in a posi- 
tion to prevent this, since the patients, who believe implicitly 
in the rheumatic nature of their pains, use them at random 
without his orders often for months and years. There are a 
great many tabetics who during the course of their disease 
have taken many hundreds of steam baths, without perceiving 
the slightest benefit therefrom. 

From the springs we can, on the whole, expect but little, 
and especially old cases with paraplegia and severe bladder 
troubles should be spared the trial. The disadvantages, the 



TABES DORSALIS. 



635 



overexertion attendant upon the journey, and the lack of home 
comforts, in the case of these patients especially, will far out- 
weigh any good results obtained from the baths ; nor should 
we, as we said above, leave out of sight the necessary cost 
which, even with the most modest pretensions, is not incon- 
siderable. One should never forget that the disease is likely 
to last a very long time, that the patient will soon be unable 
to earn any money, and that for him there can be no greater 
misfortune than to find that, heedlessly or yielding to over- 
persuasion, he has spent all his worldly goods of which now 
he stands in the greatest need. There exist not a few of such 
helpless patients in whose cases just this point was overlooked, 
and it is especially our younger colleagues who seem rather too 
prone to disregard it. If such and other objections do not exist, 
it is most advisable to recommend places where warm brine 
baths can be taken, as in Rehme-Oeynhausen, this place having 
become famous for the treatment of tabes especially, though it 
is my experience that patients get along there no better and no 
worse than at other springs of the same kind— e. g., Nauheim 
— and it only deserves to be warmly recommended owing to 
the excellent arrangements which we there find, particularly 
the facilities for moving helpless invalids from place to place. 
Chloride-of-sodium springs containing iodine and bromine — 
for instance, Konigsdorf-Jastrzemb, Kreuznach, Goczalkowitz, 
Krankenheil — may be tried without fear of doing any harm ; 
while the nonmedicated hot springs of Gastein, Teplitz, Johan- 
nisbad, Warmbrunn, Pfaffers, and the hot sulphur springs of 
Landeck, Aachen, Trentschin, Pistyan, Baden near Vienna, and 
Baden in Switzerland should be prescribed only with great 
caution, and the baths should never be taken too warm, never 
above a temperature of 8o° to 90 F. Among the chalybeate 
springs, first Cudowa, then Pyrmont, Flinsberg, Schwalbach, 
and St. Moritz (Engadine) deserve to be tried. 

The results of massage in the treatment of tabes are not sat- 
isfactory. There is no objection to giving massage in a care- 
ful manner so as to improve the nutrition of the muscles and 
to stimulate metabolism, especially in cases of young, compar- 
atively robust patients ; but we are hardly justified in building 
much upon such a procedure and in expecting to bring about 
a lasting improvement in the sensory or motor disturbances. I 
have known instances in which the general condition of the 
patient was influenced for the worse by massage, and in which 



6 3 6 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



certain symptoms, especially the lancinating pains, appeared 
to be aggravated after its use. 

Of only historical interest is the operation of nerve stretch- 
ing, which, in the first half of the eighties, was by some claimed 
to be an excellent means in the treatment of tabes, the sciatic 
nerves being usually chosen for this operation. They were laid 
bare by cutting through the gluteal muscles and " stretched " 

according to different meth- 
ods. The result was in many 
cases at first very striking. 
Pains, bladder disorders, and 
anaesthesias vanished, and the 
operation was undertaken 
comparatively frequently. 
Soon, however, it was found 
that what had been regarded 
as a success was of no long 
duration, and that the old 
troubles returned, and, final- 
ly, after it had been repeat- 
edly demonstrated at the au- 
topsy (Strumpell, Rosen- 
stein) that the elongation of 
the nerves not only had not 
exerted the slightest bene- 
ficial effect upon the morbid 
process in the spinal cord, 
but that several times at the 
place where the nerve had 
been stretched a neuritis had 
developed and extended to 
the substance of the spinal cord, giving rise to a myelitis, the 
practice was given up, and can be looked upon to-day as hav- 
ing been definitely discarded. 

Finally, after a warm recommendation by Charcot, a method 
has recently again been taken up which some }^ears ago had been 
written about by Motschukowsky (Wratsch, 1883, 17-21). The 
patient is suspended by means of an apparatus (cf. Fig. 174), as 
he would be if he were going to have a plaster-of-Paris jacket 
applied, and allowed to remain so for a few minutes. 

The results obtained with this mode of treatment in the 
Salpetriere were favorable enough to induce many clinicians in 




174.— Suspension Apparatus used in 
the Treatment of Tabes. 



TABES DORSALIS. 637 

Germany, England, and America to make further trial of it, 
and at present we possess quite an imposing array of articles 
treating of the " suspension method " and the results obtained 
by it. According to some authors the cerebral, according to 
others the spinal symptoms are improved by it. The proced- 
ure is said to be without danger, but in one instance the im- 
mediate consequences were fatal ; yet we should add that in 
this case the suspension was undertaken without the physi- 
cian's supervision (Gorecki, Lyon med., 1889, 20). Althaus (cf. 
lit.) has attempted to give an explanation of the mode of action 
of this treatment. According to his opinion, the meningitic 
adhesions over the posterior columns are loosened, so that the 
nerve fibres, especially the superficial ones, gain in power of 
conduction, the sclerosed, thickened neuroglia becomes looser, 
and the pressure upon the nerve tubes is thus diminished. He 
also thinks that suspension should only be used in older cases, 
because in recent ones it might lead to inflammatory condi- 
tions. The possibility that this loosening does take place, as 
Althaus claims, can not be disproved, but this is certain, that 
for those instances in which improvement is said to have shown 
itself after only one, two, three, or ten suspensions, this theory 
affords no explanation. 

We have tried this method on one hundred and three 
patients in private practice and in eleven cases in the hospital 
wards, all of whom had tabes. Among the one hundred and 
three private cases there were twenty-one women and eighty- 
two men ; among the hospital patients there were four women 
and seven men. The number of suspensions in the different 
cases varied from three to eighty-seven, the duration of each 
being from one to five and a half minutes, and the whole treat- 
ment comprised from three to a hundred and sixteen days. 
Among the patients some were older, some more recent cases. 
The earliest period after the onset of the disease at which the 
treatment was begun was fourteen months, the latest, seventeen 
years. 

In no single instance was I able to note any marked or last- 
ing improvement. In no case was either the general condi- 
tion of the patient or the course of the disease influenced for 
the better by it, nay, even in the individual symptoms no de- 
cided improvement could be perceived. Transient diminution 
of the ataxia, transient relief from the pains or bladder trou- 
bles could be remarked, but these ameliorations were of no 



638 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



duration, and soon everything was again just as it had been 
before. The account which intelligent and unprejudiced pa- 
tients gave of themselves after the thirtieth, fiftieth, and eight- 
ieth suspension corresponded almost exactly to that which 
they had given prior to the institution of the treatment. In 
opposition to Althaus, then, it is my conviction that anatomical 
changes are not produced by suspension, but that the transient 
improvement has to be referred to the influence of suggestion. 
The patients hear of a new treatment for their incurable dis- 
ease, they subject themselves to it with much pleasure and 
confidence, and by autosuggestion produce an improvement in 
some functional impediment (for example, in the ataxia), which 
may be quite marked, but which is never lasting. Four times 
during the act of suspension I myself met with rather unpleas- 
ant accidents ; in two cases the patients lost consciousness and 
had to be rapidly taken down, and were only then with some 
difficulty recalled to life ; in two other instances severe laryn- 
geal crises appeared, so that the procedure had at once to be 
stopped. Such accidents, of course, make a very bad impres- 
sion upon the patient, and bring the results, which are in any 
case doubtful, still more into question. Careful examination 
is necessary before the suspension is used, and if there exists 
a disease of the heart or of the vessels it should under no con- 
sideration be undertaken. We need, of course, hardly add 
that while the patient is suspended he should be carefully 
watched. A final judgment as to the usefulness of the method 
can, of course, not as yet be ventured upon, because our time 
of observation has been too short ; the impression, howeyer, 
which I myself have gathered, is that suspension will be in 
vogue for a time, only to fall again into complete oblivion. 

LITERATURE. 

I. General. 

Watteville, de. Brit. Med. Journ., December 27, 1884. 

Hollis. Brit. Med. Journ., November 22, 1884. 

Althaus. Ueber Sclerose des Riickenmarks einschliesslich der Tabes dorsalis 

etc. Leipzig, 1884. Wigand. 
Adamkiewicz. Die Riickenmarksschwindsucht. Wien, 1885. Tdplitz und 

Deuticke. 
Brieger. Berl. klin. Wochenschr., 1885, xxii, 20. 
Remak. Ibid., 1885, xxii, 7. (Tabes in childhood.) 
Althaus. Brit. Med. Journ., January, 1885, 10, 31. 



TABES DORSALIS. 



639 



Basso. I disturbi funzionali del simpatico nella tabe dorsali. Ann. univ., 18S6, 

vol. cclxxv, p. 429. 
Oppenheim. Centralbl. f. Nervenheilk., 1886, ix, 11. 
White, Hale. Lancet, December, 1886, ii, 24. 
Striimpell, A. Munch, med. Wochenschr.., 1886, xxxiii, 31. 
Carlyle. Glasgow Med. Journ., October, 1887, xxviii. 
Tuczek. Centralbl. fur klin. Med., 1887, viii, 16. 
Jendrassik. Deutsch. Arch. f. klin. Med., 1888, xliii, 6. 
Oppenheim, H. Neue Beitrage zur Pathologie der Tabes dorsal. Arch. f. 

Psych, u. Nervenkrankh., 1888, xx, 1. 
Bernhardt, M. Zeitschr. f. klin. Med., 1888, xiv, 3. 
Pitres. Arch, de neur., 1888, xv, p. 337. 
Martius. Deutsche Med.-Ztg., 1888, ix, 7, p. 87. 
Mdbius. Neuere Beobachtungen iiber die Tabes. Schmidt's Jahrbiicher, 1888, 

Bd. ccxvii, p. 73. (Sixth communication; the fifth is to be found in vol. 

ccix, 1886, p. 200 et seq. ; the fourth in vol. cciii, 1884, p. 283 et seq. 
Berger, E. Die Sehstorungen der Tabes und der Versuch einer einheitlichen 

Erklarung des Symptomencomplexes. Arch. f. Augenheilk., 1889, xix, 4. 

II. Special. 

a. Symptoms. 

Oppenheim. Berk klin. Wochenschr., 1885, xxii, 4. (Affection of the vagus.) 
Ross, James. Brain, 1886, xxxiii, p. 24. (Laryngeal crises.) 
Erben. Wien. med. Bl., 1886, ix, 43, 44. (Tabes dorsalis "cerebralis.") 
Landgraf. Berk klin. Wochenschr., 1886, xxiii, 38. (Laryngeal crises.) 
Krauss, E. Berl. klin. Wochenschr., 1886, xxiii, 46. (Paralysis of the vocal 

cords.) 
Martius. Berl. klin. Wochenschr., 1887, xxiv, 8. (Paralysis of the accessorius.) 
Arnaud. Enceph., 1887, vii, 4. (Mental disturbances.) 
Suckling. Brit. Med. Journ., July 16, 1887. (Oculo-motor paralysis.) 



Bernhardt, M. Zeitschr. f. klin. Med., 1886, xi, 4. (Differential diagnosis be- 
tween alcoholism, poliomyelitis, Landry's paralysis, and tabes.) 

Oppenheim. Berl. klin. Wochenschr., 1888, xxv, 53. (Hysterical affection of 
the nervous system resembling tabes in its course.) 

Fere. Des troubles urinaires dans les maladies du systeme nerveux et en par- 
ticulier dans l'ataxie locomotrice. Archives de neur., 1884, vii, No. 20. 

Vierordt. Beitrag zur Kenntniss der Ataxic Berl. klin. Wochenschr., 1886, 21. 

Brouardel. Gaz. des hop., 1887, 1888, lx, Ixi. (Lectures on impotence caused 
by tabes, etc.) 

Rosenheim. Arch. f. Psych, u. Nervenkr., 1884, xv, 1. (Experimental studies 

on the " tendon phenomena.") 
Zenner. On the Knee-jerk in Locomotor Ataxia. Journ. of Nerv. and Ment. 

Diseases, N. S., April, 1884, ix, 2. 
Delprat. Nederl. tijdschr. v. Geneesk., 1886, 51. (Three cases of tabes where 

the knee phenomenon persisted until a few hours before death.) 



640 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Westphal. Ueber Fortdauer des Kniephanomens bei Degeneration der Hinter- 
strange. Arch. f. Psych, und Nervenkrankh., 1886, xvii, 2. 

Mitchell, Weir, and Morris. Tendon-jerk and Muscle-jerk in Disease, especially 
with Reference to Posterior Sclerosis of the Spinal Cord. New York Med. 
Record, 1886, xxx, 1. 

Krauss, E. Beitrag zur Localisation des Patellarreflexes bei Tabes u. s. w. 
Neurol. Centralbl., 1886, v, 20. 

Hirt. Ueber Tabes mit erhaltenen Patellarreflexen. Berl. klin. Wochenschr., 
1886, xxiii, 10. 

Westphal. Zwei Falle von Tabes mit erhaltenem Kniephanomen. Berl. klin. 
Wochenschr., 1887, xxiv, 5. 

Minor. Zur Frage iiber die Localisation des Patellarreflexes bei Tabes. Cen- 
tralbl. f. Nervenheilk., 1887, x, 6. 

Westphal. Anat. Befund bei einseitigem Kniephanomen. Arch. f. Psychiatrie 
und Nervenkrankheiten, 1887, xviii, 2. 

Goldflam. Ueber die Ungleichheit des Kniephanomens bei der Tabes. Neurol. 
Centralblatt, 1888, vii, 19, 20. 

Warren Plympton Lombard. The Variations of the Normal Knee-jerk and 
their Relations to the Activity of the Central Nervous System. Amer. 
Journal of Psychology, 1887, 1. 

Meyer. Berlin, klin. Wochenschr., 1888, 2. (The influence of physostigmine 
on the tendon reflexes.) 

Benedict. Qualitative Veranderungen des Kniephanomens. Neurolog. Cen- 
tralblatt, 1889, 17. 

Portalier. These de Paris, 1884. (Trophic disturbances in the preataxic stage 
of tabes.) 

Rossolymmo. Archiv f. Psych, und Nervenkrankheit., 1884, xv, 3. (Trophic dis- 
turbances of the skin.) 

Tanowsky. Wien. med. Presse, 1885, xxvi, 8. (The exanthemata of tabetics.) 

Hoffmann. Berliner klin. Wochenschrift, 1885, xxii, 12. 

Browne and d'Arcy Power. St. Barthol. Hosp. Rep., 1886, xviii. (" Mai per- 
f or ant dn pied."} 

Galippe. Gaz. des hop., 1886, 58. (Affections of the teeth.) 

Kronig. W r irbelerkrankung der Tabiker. Deutsche Med.-Ztg., 1886, vii, 101. 

Hinze. Das Plantargeschwiir und sein Verhaltniss zur Tabes. Petersburger 
med. Wochenschr., N. F., 1886, iii, 26-28. 

Menetrier. Ann. de dermatologie, 1886, vii, 1. (" Mai p erf or ant" on the hands.) 

Molliere. Lyon med., 1887, Iv, p. 377. (Tabes beginning with trophic disturb- 
ances.) 

Suckling. Brit. Med. Journ., April 6, 1885. (Perforating ulcer as the first symp- 
tom of tabes.) 

Marshall, J. G. Lancet, January, 1885, i, 1. 

Joffroy. Gaz. des hop., 1885, 133. (Tabetic foot.) 

Richardiere. Revue de med., February 2, 1886, vi. (Arthropathy in the finger 
joints.) 

Anderson, J. Wallace. Brain, 1886, xxxiv, p. 224. (Arthropathy.) 

Kosinzow. Med. Observ., 1886, 17. 

Lowenfeld. Munchener med. Wochenschr., 1887, xxxiv, 20. (Arthropathy.) 



TABES DORSALIS. 



641 



Rotter. Arch. f. klin. Chirurgie, 1887, xxxvi, 1. (Arthropathy in tabes.) 

Kramer. Prager med. Wochenschr., 1887, xii, 33. (Tabetic foot.) 

Kahlden. Virchow's Archiv, 1887, cix, 2. (Arthropathy.) 

Porter. New York Medical Record, October, 1887, xxxii, 18. (Arthropa- 
thy.) 

Dana. Boston Medical and Surgical Journal, October 17, 1887, cxvii. (Ar- 
thropathy.) 

Paolides. Des arthropathies tabetiques du pied. Neur. iconogr. de la Salpetr., 
1888, 4, 5. 

Collier and Pitt. Transactions of the Pathological Society, 1888, xxxix, p. 22. 
(Charcot's disease of the knee-joint.) 

Kredel. Die Arthropathien und Spontanfracturen bei Tabes. Volkmann'sche 
Sammlung klin. Vortrage, 1888, 309, Chir. No. 96. 



Sakaky. Arch. f. Psych, und Nervenkrankh., 1884, xv, 2. (Degeneration of the 

peripheral nerves.) 
Stern, Bolko. Ibid., xvii, 3. (Abnormities in sensation.) 
Remak. Berlin, klin. Wochenschrift, 1887, xxiv, 19. (Neuritic atrophy in 

tabes.) 
Oppenheim and Siemerling. Arch. f. Psych, und Nervenkrankh., 1887, xviii, 2. 

(Affection of the peripheral nerves.) 
Dejerine. Gaz. med. de Paris, 1888, 10, II, 12. 
Dejerine. Revue de med., 1889, ix, 2, 3, 4. 
Dejerine et Sollier. Arch, de med. experiment., 1889, 1, 2. 

Complications. 

Oppenheim. Berl. klin. Wochenschr., 1884, xxi, 38. (Hemicrania.) 
Leichtenstern. Deutsche med. Wochenschr., 1884, x, 52. (Pernicious anaemia 

in tabes.) 
Oppenheim. Berl. klin. Wochenschr., 1885, xxii, 49. (Diabetes mellitus with 

tabes.) 
Reumont. Ibid., 1886, xxiii, 13. (Diabetes mellitus with tabes.) 
Grasset. Arch, de neurol., July, 1886, xii. ("Tabes combine," myelite 

mixte.) 
Fischer. Centralblatt der Nervenheilk., 1886, ix, 18. (Diabetes mellitus with 

tabes.) 
Leyden. Centralbl. f. klin. Med., 1887, viii, 1. (Cardiac affections in tabes.) 
Eulenburg. Deutsche med. Wochenschr., xiii, 35. (Tabes combined with 

motor system diseases of the spinal cord.) 
Grodel. Deutsche med. Wochenschrift, 1888, xiv, 25. (Cardiac affections in 

tabes.) 
Stransky. Prager med. Wochenschrift, 1888, xiii, 25. (A case of tabes com- 
plicated with muscular atrophy.) 
Eulenburg. Virchow's Archiv, 1885, xcix, 1. 
Berger, O. Breslauer arztliche Zeitschrift, 1885, vii, 1, 3-5. 
Wilks. Brit. Med. Journ., February 6, 1886. 
Buzzard. Brit. Med. Journ., January 30, 1886. 
Striimpell. Neurol. Centralblatt, 1886, v, 19. 
41 



642 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Rumpf. Deutsche med. Wochenschr., 1887, 36. 
Neumann. Berl. klin. Wochenschr., 1887, xxiv, 43. 

b. Pathological Anatomy. 

Lissauer. Neurol. Centralbl., 1885, iv, 11. 

Krauss, E. Neurol. Centralbl., 1885, iv, 3. 

Adamkiewicz. Die anatomischen Veranderungen bei Tabes. Congr. interna- 
tional de Copenhague, iii, Psych, u. Neurol., 1886, p. 9. 

Mitchell, S. Weir. Locomotor Ataxia confined to the Arms ; Reversal of Or- 
dinary Progress. Journal of Mental and Nervous Diseases, N. S., April 4, 

1888, xiii. 

Dejerine. Contribution a l'etude de l'ataxie locomotrice des membres superi- 

eures. Arch, de Phys., 1888, 4me ser., 1, 3. 
Pick. Arch. f. Psych, und Nervenkrankh., 1889, xx, 3. (Anatomical changes 

in a case in which the knee-kick was absent on one side only.) 

c. ^Etiology. 

Eisenlohr. Deutsche med. Wochenschrift, 1884, x, 52. 

Stephan. Nederl. Weekbl., 1885, 51. 

Straus. Faits pour servir a l'etude des rapports du traumatisme avec le tabes. 
Arch, de Phys., November 8, 1886, xviii. 

Minor. Contribution a l'etude du tabes. Arch, de neurol., 1889, 50, p. 183; 
51, P- 362. 

d. Treatment. 

Rumpf. Allgem. Wiener med. Zeitg., 1886, 6, 7. 

Lehmann. Deutsche med. Wochenschr., 1886, xii, 4. (Recovery from tabes.) 

Schurigin. Wratsch, 1886, 15. (Static electricity.) 

Eulenburg. Die Heilbarkeit der Tabes dorsalis. Congres intern, de Copen- 
hague, iii, Psych, u. Neurol., 1886, p. 71. 

Rigal. Gaz. des hop., 1886, 74. (Deep cauterization of the vertebral col- 
umn.) 

Benedikt. Ueber Prognose und Therapie der Tabes. Wiener med. Presse, 
1887, xxviii, 33, 34. 

Lyman. Journal of Mental and Nervous Diseases, July 7, 1887, xiv. 

Stembo. Berl. klin. Wochenschr., 1888, xxv, 44 

Naunyn. Mitth. aus der med. Klinik zu Konigsberg in Preussen. Leipzig, 1888. 
(Subcutaneous injections of strychnine.) 

Benedikt. Wiener med. Blatter, 1889, xii, 8. (Nerve stretching.) 

Treatment by Suspension. 
Charcot. De la suspension dans le traitement de l'ataxie locomotrice progres- 
sive et de quelque? autres maladies du systeme nerveux. Progr. med., 

1889, 3. 

Weir Mitchell. Medical News, April 13, 1889. 

Chernel. Wiener med. Blatter, 1889, xii, 5. 

Dana. New York Med. Record, April 15, 1889. 

Gilles de la Tourette. Progr. med., 1889, xvii, 8. (Technique of suspension.) 

Morton. New York Med. Record, April 15, 1889, xxxv. 



TABES DORSALIS. 643 

Althaus. Lancet, April 13, 1889, p. 160. 

Watteville. On the Treatment by Suspension of Locomotor Ataxy. London, 

1888. 
v. Openchowski. German translation of Motscherkowski's original article. Berl. 

klin. Wochenschr., 1889, 25. 
Ladame. Revue med. de la Suisse romande, 1889, 6. 
Eulenburg und Mendel. Berl. klin. Wochenschr., 1889, 8. 
Bernhardt. Neurol. Centralbl., 1889, 11. 
Gilles de la Tourette. Arch, de neurol., July, 1889, xviii, No. 52. 



CHAPTER III. 

DEMENTIA PARALYTICA PROGRESSIVA GENERAL PARALYSIS OF THE 

INSANE GENERAL PARESIS — SOFTENING OF THE BRAIN. 

While in tabes we have learned to recognize a disease of 
the general nervous system, in which the spinal cord chiefly is 
the affected portion, we find that in dementia paralytica, on the 
other hand, the brain is above all the part attacked, whereas 
the spinal cord and the peripheral nerves do not suffer so regu- 
larly nor to so marked a degree. In its distribution the lesion 
of the cord is either diffuse or, as in tabes, confined to the pos- 
terior columns. With regard to the affections of the spinal 
nerves a more careful study is still necessary, and more espe- 
cially this question needs to be answered whether here, as 
seems indeed very probable, primary degenerative processes, 
analogous to those of tabes, can also be demonstrated. 

./Etiology. — The manifold points of resemblance between 
general paralysis and tabes, to some of which we have drawn 
attention above, are found first in the aetiology of the two dis- 
eases. In the former as well as in the latter hereditary tenden- 
cies are of much significance. A person belonging to a family 
in which nervous diseases of any kind have been prevalent is 
more prone to develop general paralysis than a member of a 
healthy family. However, this factor is in the majority of in- 
stances not sufficient in itself to bring about the disease, certain 
exciting causes being also necessary, and experience has taught 
us that it is chiefly overstrain of the nervous system, and more 
especially of the brain, which favors its development. Such 
excessive demands which are made upon the brain are numer- 
ous. Chief among them is mental overstrain, caused by too 
close attention to work and worrying over business— too much 
scheming, calculating, etc. — so that we are not surprised that 
bookkeepers, accountants, bankers, stock brokers, authors, 
actors, etc., form the relatively largest contingent of cases. 



DEMENTIA PARALYTICA. 



645 



Besides this, deep emotions, repeated or long-lasting sorrows 
or care, the struggle for existence, disappointed hopes, baffled 
ambitions, and fright, may obtain ^etiological importance. On 
hearing the history of a general paralytic, one at least of these 
factors will hardly ever be absent. Bodily overstrain, forced 
marches, excesses in Venere and the like, can be made respon- 
sible to a less extent. Excesses in Baccho, the habitual abuse 
of alcohol, only rarely lead to general paralysis, but sometimes 
a condition is produced by such excesses, the " pseudo-paralysis 
a potu," which resembles general paralysis, but which is quite 
distinct from it, and belongs to chronic alcoholism. There is 
no question but that the occupation may furnish causes for the 
disease ; thus, those which entail at once bodily and mental 
work, or those in which the workers must for a long time re- 
main in very hot rooms, and again the working in poisons, 
especially in lead (Snell, Vogel, and others), are particularly 
dangerous. Of great interest, finally, is the fact that, like 
tabes, general paralysis may be caused by traumatism either to 
the head or the back, so that we have a traumatic progressive 
paralysis which is quite analogous to the traumatic tabes. In 
this latter category we must also place the insolation, sun- 
stroke (heat stroke) which has been known to lead to general 
paralysis (Bonnet and Paris, Ann. med.-psych., November, 1884, 
6, S. 12). 

Besides the congenital, however, there exists also an ac- 
quired predisposition, which differs from the former, inasmuch 
as no other exciting causes are needed for the production of 
the disease, but that, just as is the case in tabes, it alone is suffi- 
cient to bring about general paralysis. We refer, of course, to 
syphilis. The same highly important role which it plays in 
tabes it plays here too. An individual who has had syphilis 
has much greater cause to fear general paralysis than one who 
has never been infected. According to the statistics of Rieger 
(cf. lit), the one is sixteen or seventeen times as liable to the 
disease as the other. These figures correspond about to those 
founded on my own experience. Out of two hundred and 
fifty-seven paralytics a hundred and seventy-one had been 
syphilitic, and out of two hundred and sixty patients with 
other diseases only fourteen. Heredity and all the exciting 
causes taken together do not give rise to as many cases of pa- 
ralysis as syphilis alone ; but here again, as in tabes, we must 
leave the question open as to how syphilis acts, whether, as we 



646 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

think ourselves, the syphilitic arterial disease is responsible, or 
whether we are dealing with a toxic action (cf. page 624), so 
that general paralysis has to be regarded as a post-syphilitic 
affection. Whatever we decide about this, the fact that gen- 
eral paralysis may be the result of syphilis is universally ac- 
knowledged, and the numerous writings which we possess on 
the subject are all without exception in favor of this view. 

The influence which has been ascribed to age and sex can 
usually be explained by that of syphilis. Males are more fre- 
quently attacked than females, the ratio being seven men to 
two women. Those in the prime of life furnish the largest 
contingent. 

Symptoms. — The symptoms of the disease are partly psy- 
chical, partly somatic, and this will not surprise us when we 
learn that the seat of the affection is preferably in the brain, 
and more particularly in the psycho-motor region of the cere- 
bral cortex. The psychical manifestations differ very greatly, 
and it is more especially in the prodromal stage that these 
variations are most noticeable. This is a feature equally well 
marked here as in tabes, and the main difference between the 
two consists in the fact that in general paralysis the clinical 
picture of the prodromal stage is dominated by the psychical 
manifestations. The patient becomes unable to concentrate 
his mind for any length of time. He gets easily fatigued when 
he has exerted himself mentally, he becomes forgetful, and is 
no longer able to comprehend and deal with matters which he 
previously understood perfectly. He is found to be indifferent 
in the performance of his duties and careless in keeping his ap- 
pointments ; he becomes unreliable and absent-minded. When 
writing, he makes mistakes in spelling, and presents a slowness 
in thinking and a general dullness of intellect which are quite 
foreign to him. At the same time his disposition presents 
alterations. Previously tolerant and kind, he becomes now ill- 
humored, moody, and irritable ; on the slightest provocation 
he loses his temper and may even be inclined to violence. His 
character is not the same as it was ; his will power becomes 
weak ; he loses his energy and his moral individuality ; he 
allows himself to be influenced and overpersuaded by anybody, 
and even thus early does things for which he can give no clear 
motive ; he gradually loses all consideration for others in his 
social intercourse ; he neglects his appearance, his dress looks 



DEMENTIA PARALYTICA. 647 

untidy, he becomes indecent, commits nuisances on the open 
streets, tells obscene stories before his children, and so forth. 
In exceptional cases the patient himself is to a certain extent 
conscious of these changes which are going on in him. They 
surprise him, and he speaks about it to his most intimate friends 
and expresses a fear that some serious disease is coming on; 
but in the great majority of cases, he does not in the least ap- 
preciate his condition, which worries and troubles his family 
so much. Months, even years, may thus pass and no new mani- 
festations make their appearance. It is only the occurrence of 
certain somatic symptoms which gives to the clinical picture 
a different aspect. Among these latter there are especially 
two on account of which the physician is consulted, namely, 
insomnia and the alteration in speech. The former is all the 
more striking because the patients often by day and at their 
work are overpowered by sleep, while at night they lie awake 
for hours without being able to rest. The latter manifests 
itself by a difficulty in pronouncing certain words. The pa- 
tient stutters, misplaces letters and syllables, leaves syllables 
out, in a word, presents the group of symptoms known as 
" syllable stumbling " {Sylbenstolpern). At the same time the 
voice loses its usual timbre ; it becomes harsh and its former 
modulation is gone. 

For the examining physician, the associated movements in 
the facial muscles, the fibrillary tremor and twitching of the 
lips, and the tremulousness of the protruded tongue are suffi- 
cient to lead him to the diagnosis, and the inequality of the 
pupils which may appear at this stage is an important sign. 
The motor disturbances further manifest themselves in a change 
in the handwriting and in the gait. The writing shows uncer- 
tainty and irregularity ; the letters, which are usually larger 
and written more awkwardly than before, become tremulous ; 
the paper is covered with blots ; the words are incorrectly 
written, inasmuch as letters or entire syllables are omitted or 
misplaced. The gait becomes awkward and clumsy and the 
patient " shuffles along " ; he is one-sided, and small obstacles 
in his path are apt to cause him to fall. 

This initial stage, which in its duration varies from a few 
months to one, even two or three years, is followed by a stage 
which is mostly characterized by a rapid increase in the psy- 
chical excitement (" maniacal exaltation "). The patient — pre- 
viously quiet, sullen, apparently occupied with his own 



648 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

thoughts — now becomes noisy, talkative, all the time restless 
and in a state of excitement ; without noticing his surround- 
ings and his friends, he lives with a sense of perfect comfort ; 
he is young, handsome, extremely strong, and immensely rich; 
he has studied all sciences ; he occupies himself with absolutely 
preposterous but to him feasible schemes ; he is going to dry 
up the Atlantic Ocean, he is the Emperor of China, he is Na- 
poleon, Christ, he is the chief among the gods, etc. In the 
dreamlike play of his imagination all these fantasies arise, but 
the patient is not able to give them any logical connection. 
Without critical faculty he stands out a pitiable victim of the 
most bizarre delusions of grandeur. At the same time his 
memory rapidly fails him, especially for recent events ; what 
he did to-day, yesterday, the last visit of the physician, etc., he 
does not remember, whereas the reminiscences of long-past 
years can still be called up. He does not know the day of the 
week or even the name of the month and the season in which 
he is at present. People with whom he used to deal in busi- 
ness he no longer recognizes ; he confounds them with other 
persons, etc. The lack of judgment of the patient has, of 
course, a decided influence upon his actions ; he buys things 
recklessly, squanders his money in a most foolish manner, he 
makes debts, commits easily discoverable frauds, which he de- 
nies with the utmost calmness when he is found out. Assaults 
of which he may be guilty, misdemeanors against the public 
order, offenses against the public morals, etc., not infrequently 
lead to trouble with the authorities and to the arrest of the 
patient. 

In by far the smaller number of cases the above-described 
initial stage is followed, instead of by the maniacal exaltation, 
by a stage of depression. The patient believes himself perse- 
cuted by everybody, and his life menaced ; he hears voices, and 
he is always troubled with a presentiment that something ter- 
rible is going to happen. He cries, laments, begs for help, and 
so forth. In other instances hypochondriacal delusions gain 
the upper hand. The patient imagines that he is made of 
glass, that he can not eat, that he is unable to urinate, that he 
has no head, and the like. The lack of all power of criticism 
in these delusions, and the inability to systematically elaborate 
them, and the usually rapid course of this stage, distinguishes 
the general paralytic from the insane patient. 

Quite gradually in the course of time the general aspect 



DEMENTIA PARALYTICA. 649 

changes, the excitement abates and disappears, and the intel- 
lectual impotency increases. The patient spends his days with- 
out a thought or care, writing and reading become to him lost 
arts, he forgets his own name, and his social position, he be- 
comes oblivious of his family, and in general takes no interest 
whatever in the outside world. This is the stage of dementia. 
He becomes uncleanly in his habits, his eating and drinking 
must be watched, and step by step the psychical life approaches 
more and more its extinction ; the patient no longer lives, he 
vegetates. 

It is of great practical importance and interest to study 
the somatic disturbances which occur in the course of the dis- 
ease associated with the psychical ones, and which are caused 
by the simultaneous affection of the spinal cord (and periph- 
eral nerves). The diminution of sensibility, that of the skin 
as well as of the nerves of special sense, particularly of the 
opticus, the absolute inactivity of the pupils, the decrease in 
the perception of pain, the changes in the electrical excitabil- 
ity of the muscles, which at first is increased, later diminished, 
the (not regular) loss of the tendon reflexes, the appearance of 
trophic disturbances, the tendency to bedsores, the perforating 
ulcer of the foot (inal perforant du pied, cf. page 610), all point 
to a participation of the spinal cord in the morbid process. 
Sometimes, quite early, peculiar attacks occur, which, asso- 
ciated with loss of consciousness, are either accompanied by 
transient hemiplegias or convulsive movements, and which 
therefore either deserve the name of apoplectiform or epilepti- 
form seizures. They are designated as " paralytic attacks " 
par excellence. Under certain circumstances they appear very 
frequently, from ten to fifty times in one day, and they may 
then keep the patient in an almost constant condition of un- 
consciousness. The elevation of temperature which accom- 
panies these attacks is not considerable, the occurrence of 
albumen in the urine not constant. Among the affections of 
the cranial nerves which have been but little studied in their 
connection with general paralysis, there is particularly the 
optic atrophy, which is seen in ten per cent of all cases. The 
nerves of the ocular muscles also frequently become attacked, 
the implication of the trigeminus and of the facial being less 
common. Of the nuclear affections of the vagus coming on in 
the course of this paralysis nothing definite is known. 

The duration of the disease varies much. In the "galloping 



650 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



form," in which, owing to the sleeplessness and inability to take 
sufficient food, the strength rapidly fails, it may require only a 
few months to bring about a fatal issue. At other times the 
disease may last two, three, five, or even more years, out of 
which no small proportion is liable to be spent in an asylum, 
as it is positively impossible to keep the patient at home, in 
spite of all the care and devotion possible on the part of the 
family. 

Pathological Anatomy. — The questions as to the anatom- 
ical nature of the disease have unfortunately not been as yet 
answered satisfactorily, and there is still a great deal of diver- 
sity of opinion among the authorities on this point, although 
the macroscopical appearances are usually very characteristic, 
the atrophy of the brain, especially in the anterior regions, 
being very striking. Although no one can doubt that the con- 
volutions are diminished in size, that the frontal and the parie- 
tal lobes weigh less than in a normal brain, yet the precise 
mode in which this atrophy comes about, what are the micro- 
scopical changes in the nerve elements of the cortex, and what 
is the primary process in all this, is not as yet decided, but re- 
mains the subject of much controversy. According to Tuczek, 
there is a marked primary atrophy of the fine medullated nerve 
fibres, particularly in the outer layers of the cortex, in the 
tangential " association " fibres, which run parallel to the sur- 
face. The gyrus rectus is said to be relatively the earliest 
attacked, later, the remaining frontal brain and the island of 
Reil, then the temporal, but the occipital lobes never. This 
view, according to which the atrophy is the primary process, 
is in all probability correct, although it is still combated by 
many authorities (Mendel), who look upon the death of the 
nerve fibres as the secondary, upon the increase of the con- 
nective tissue, the thickening of the vessel walls, and the ap- 
pearance of spider cells, as the primary process (" encephalitis 
interstitialis "). 

Analogous changes in the ganglionic cells have frequently 
been noted (Binswanger, Mendel, Gudden) ; a peculiar aggre- 
gation of nuclei associated with disease of the vessels, changes 
in the bodies of the cells in the large pyramids of the para- 
central lobule, changes in the nucleoli and nuclei, and sclerosis 
and atrophy of the cells are not uncommonly found in this 
connection. 

But, besides the cortex, the deeper regions also are the 



DEM EN TIA PA RA L Y TIC A . 



6 5 I 



seat of alterations, and the manifold changes, which the white 
matter of the hemispheres may undergo, have been studied 
among others by Friedmann. He describes four different 
forms of atrophy of the fibres of the white matter, the number 
of the fibres diminishing in a manner analogous to that which 
has been shown by Tuczek to be true for the cortex. The 
central ganglia of the brain do not remain exempt, nor, as 
Westphal has shown, are the pyramidal tracts or the posterior 
columns of the spinal cord spared. Fascicular degeneration 
occurs in them also, a fact which probably accounts for a not 
inconsiderable part of the motor disturbances. 

The condition of the pia varies. Frequently it is adherent 
over large areas of the underlying cortex, so that it can not 
be stripped off without loss of substance ("decortication"). In 
rare instances, although it is nowhere adherent, in places it is 
thickened, of greater consistence than normal, and contains 
variable amounts of fluid in its meshes. Whether the latter 
condition is only a later stage of the former — that is, whether 
adhesions only exist at first, but later disappear — is not defi- 
nitely known. 

A case recently reported by Rey (cf. lit.) shows that excep- 
tionally all the symptoms of progressive paralysis of the insane 
may be observed during life, and yet at the autopsy no change 
be found. The same thing, as we have mentioned, has been 
known to occur in connection with multiple sclerosis. 

Diagnosis. — The diagnosis may present some difficulty, inas- 
much as in certain forms of chronic alcoholism the egoism may 
also be exaggerated as in general paralysis, and inasmuch as 
cerebral syphilis, brain tumor, senile dementia, finally, chronic 
meningitis and multiple sclerosis, may more or less resemble 
general paralysis in their course and their symptoms. In al- 
coholism the hallucinations are wont to be a prominent feature, 
the speech disturbances are less marked, and the ideas are 
worked out in a more connected manner. The tremor and the 
history in cases of chronic alcoholism will also assist us in our 
diagnosis. In cerebral syphilis also the history as well as the 
age of the patient (who is, as a rule, younger than the para- 
lytic) must be taken into consideration. Brain tumors present 
a similarly progressive course, but the stage of exaltation is ab- 
sent and the characteristic delusions of grandeur do not occur ; 
in place of them we have stupor and somnolence. Senile de- 
mentia, of course, occurs in people of advanced age, and is 



652 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

characterized by a tendency of the process to remain stationary 
for some time. 

In meningitis we have febrile symptoms ; the choked disks, 
which are found comparatively frequently here, and the de- 
lirium which occurs early will guard us against errors. In 
multiple sclerosis, finally, we have the scanning speech and 
the intention tremor, and in cases where the disease is well 
developed, it can not be mistaken for general paralysis. In 
certain forms, however, the differentiation may be impossible. 
The most important points to be remembered in the diagnosis 
of general paralysis are, then, the following : The pronounced 
psychical weakness, which even in the initial stages is the 
most prominent feature of the disease ; the constantly progress- 
ive course; the motor as well as the sensory changes, the 
former of which give rise to more or less marked alterations in 
the speech, the hand-writing, and the walk, the latter to changes 
in the impressionability to external stimuli and to marked in- 
terference with the functions of the nerves of special sense — the 
cutaneous sensibility, the sense of taste, hearing, and smell. 
With this in mind we shall make a correct diagnosis at least 
in a good many cases ; to avoid errors completely will be im- 
possible even to the most experienced. 

Prognosis. — We need hardly say much about the prognosis. 
From the above description we can well infer how unfavorable 
it must be. Almost all cases prove fatal in a few years, and 
the outlook for complete recovery is worse here than in tabes. 
To be sure, it has been claimed that such may occur in pro- 
gressive paralysis (Wendt, Voisin), but, in the instances in 
which it was observed, the possibility that the case was not 
one of dementia paralytica, but rather one of the so-called 
pseudo-paralyses, such as are known to occur after the abuse 
of alcohol, can not be excluded with certainty. 

Treatment. — In the treatment of the disease we must chiefly 
endeavor to keep away all excitement from the patient, and, 
since this is best and most easily accomplished in an asylum, it 
is the first duty of the physician, after he has once made the 
diagnosis definitely, to urge the family to transfer the patient to 
some such institution. Only then is it possible to guard the 
patient as well as the family against all the accidents and fatali- 
ties to which he is otherwise necessarily exposed. This step 
must be taken as early as possible, not with the idea that the 
patient will be cured, but with the conviction that only in an 



DEMENTIA PARALYTICA. 653 

institution is he safe, and that there alone it will be possible to 
secure for him the proper care and nursing so necessary for 
one in his condition. Where there is a history of syphilis, the 
treatment with inunctions must of necessity be given a trial, 
however slight may be the prospect of success. Once decided 
upon, let the antisyphilitic treatment be pursued with vigor ; 
at Least three to four hundred grammes (gix-^xij) of mercu- 
rial ointment should be used altogether, to which must be 
added from two to three grammes (grs. xxx-xlv) of the iodide 
of potassium daily for a good while. To meet the outbreaks 
of exaltation and the insomnia the usual hypnotics, which are, 
however, of little avail, should be tried. Sulphonal in doses of 
two or three grammes (grs. xxx-xlv), methylal in doses of from 
five to eight grammes (grs. lxxv-3ij), by the mouth (Mairet 
and Combemale), morphine, from one and a half to three centi- 
grammes (grs. %-%) hypodermically, chloral, paraldehyde, pos- 
sibly also hyoscyamine, should be tried in turn. The cold- 
water treatment and baths, also galvanism to the brain, are 
decidedly contraindicated. All such procedures are likely only 
to increase the excitability of the patient, to give him all kinds 
of unpleasant sensations, and to make his troubles worse, with- 
out being in any way of benefit to him or relieving his condi- 
tion. 

LITERATURE. 
a. Symptoms. 

Christian. Ann. med. -psych., 1884, 6me ser., xii, 1. (Difficulties in diagnosis.) 

Camuset. Ibid., 1884, 6me ser., xi. (Hysterical crises.) 

Eckholdt. Allgemeine Zeitschrift fur Psychiatric 1884, xli, 1. 

Hitzig, E. Berliner klin. Wochenschrift, 1884, xxi, 33. (Subnormal tempera- 
tures.) 

Westphal. Deutsche med. Wochenschrift, 1884, x, 30. (With simultaneous 
spinal disease and blindness.) 

Wagner, Jul. Zur Kenntniss der Riickenmarkserkrankung der Paralytiker. 
Wien. med. Jahrbuch, 1884, 2, 3. 

Thomsen. Charite-Annalen, 1886, xi, p. 339. (Argyll-Robertson pupil.) 

Moeli. Arch. f. Psych, und Nervenkrankheiten, 1887, xvii, 1. (Argyll-Robert- 
son pupil in progressive paralysis of the insane.) 

Greppin. Ibid., 1887, xviii, 2. 

Kirn. Ueber Lesestorungen bei paralytischen (und nicht paralytischen) Geistes- 
kranken. Inaugural Dissertation. Miinchen, 1887. 

Acker. Allgem. Zeitschr. fur Psychiat., 1887, xliv, 1. (Report of cases.) 

Bonnet. Arch, de neurologic 1887, xiv, p. 79. (Report of cases.) 

Folsom, Charles. Boston Med. and Surgic. Journal, September 9, 1887, cxvii. 
(Early symptoms.) 



654 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Striimpell. Neurolog. Centralblatt, 1888, 5. (General paralysis combined with 

tabes in a child after syphilis of the father.) 
Jelly. Boston Med. and Surgic. Journal, July 2, 1888, cxix. (Duration of ten 

years.) 
Rottenbiller. Centralbl. f. Nervenheilkunde, 1889, xii, 1. (Observations of the 

temperature.) 
Buchholz. Das Verhalten der Pupillen bei Dementia paralytica. Inaugural 

Dissertat. Breslau, 1889. 
Wendt. Allgem. Zeitschrift f. Psych., 1889, xlvi, 1. (Recovery.) 
Voisin. Bull, de therapeut., May 15, 1889. (Curability of general paralysis.) 
Gerlach. Arch. f. Psych, u. Nervenkrankheiten, 1889, xx, 3. (Changes in the 

galvanic excitability.) 
Ascher. AUgem. Zeitschr. f. Psych., 1889, xlvi, 1. (Course and aetiology of 

general paralysis.) 
Godet. Revue med. de la Suisse Rom., April, 1889, ix, 4. (Pseudo-paralysis 

caused by alcoholic excesses.) 
Fiirstner. Munch, med. Wochenschr., 1886, xxxiii, 22. (Spinal affections.) 
Pelizaeus. Neurol. Centralbl., 1886, v, 10. (Rare initial symptoms.) 
Rey. Ann. med. -psych., May 3, 1886, 7me ser., iii. (Ataxia of the upper ex- 
tremities and hemiplegia.) 
Rosenthal. Centralblatt f. Nervenheilkunde, 1886, ix, 8. (Sensory aphasia.) 

b. Pathological Anatomy. 

Tuczek. Beitrag zur pathologischen Anatomie und Pathologie der Paralyse. 

Berlin, Hirschwald, 1884. 
Zacher. Arch. f. Psych, und Nervenkrankheiten, 1884, xv, 2. 
Savage. Journal of Mental Sc, January, 1884, xxix. (Pachymeningitis and 

paralysis.) 
Camuset. Annal. medico-psychol., November, 1884, 6me ser., xii. (Changes 

of the dura mater in paralysis.) 
Mendel. Allgem. Zeitschr. f. Psych., 1885, xii, 4, 5. (The ganglionic cells of 

the brain cortex in general paralysis.) 
Baillarger. Ann. med.-psychol., 1886, xliv, 1. (Diminution in weight of the 

cerebrum.) 
Tschish. Wojenn. Med. Sh., January, 1886. 
Meynert. Von Mechanismus der progressiven Paralyse. Wien. med. BL, 

1887, x, 17, 18. 
Zacher. Das Verhalten der markhaltigen Nervenfasern u. s. w. Arch. f. Psych. 

und Nervenkrankh., 1887, xviii, 1. 
Zacher. Arch. f. Psych, und Nervenkrankh., 1888, xix, 3. (General paralysis 

associated with focal lesions in the internal capsule.) 
Rey. Ann. med.-psych., March, 1889, 7me ser., ix, 2. (During life symptoms 

of general paralysis ; at the autopsy no changes found.) 
Binswanger. Allg. Zeitschr. f. Psych., 1886, xlii, 4. (Pathological histology.) 

c. JEtiology and Occurrence. 

Snell. Allgem. Zeitsch. f. Psych., 1884, xii, 3. (General paralysis and chronic 

lead poisoning.) 
Frankel. Ibid., xii, 1. (General paralysis in women.) 



DEMENTIA PARALYTICA. 655 

Mabille. Ann. med. -psych., 1885, yme ser., i, 3. (Traumatism.) 

Bonnet. Ibid., 1884, 6me ser., xii. (Insolation.) 

Vogel. Zwei Falle von allgem. progressiver Paralyse nach chron. Bleiver- 
giftung. Dissert. Inaugur., Bonn, 1886. 

Rieger. Statistische Untersuchungen iiber den Zusammenhang Zwischen Syphi- 
lis und progressiver Paralyse. Schmidt's Jahrbiicher, 1886, vol. ccx, p. 88. 
(Contains numerous references.) 

Preuss, Jul. Inaugural Dissertat. Berlin, 1886. (On syphilis and dementia 
paralytica.) 

Brie, Paul. Inaugur. Dissert., Breslau, 1886. (On syphilis and dementia para- 
lytica.) 

Nasse. Zeitsch. f. Psych., 1886, xlii, 4. 

Ball. Congr. internat. de Copenhague, iii, Psych, and neurol., p. 76. (Heredity.) 

Christian. Arch, de neurol., 1887, xiv, p. 205. (^Etiology of the disease in the 
male.) 

Vernet. La syphilis est-elle une cause de la paralysie generale? These de 
Nancy, 1887. 

Levinstein. Beitrag zur Aetiologie und Therapie der Dem. paralytica. Dissert. 
Inaugural, Berlin., 1887. 

Regis. Gaz. de Paris, 1888, 7me ser., v, 23, 24, 26 (Relation between gen- 
eral paralysis and syphilis.) 

Mesnet. Bull, de l'Acad. de med., 1888, 3me se>., xx, 46. (Relation between 
syphilis and general paralysis.) 

Siemerling. Statistisches und Klinisches zur Lehre von der progressiven Pa- 
ralyse der Frauen. Charite-Annalen, 1888, xiii, p. 392. 

Ball. De la paralysie generale de l'origine traumatique. Encephal., 1888, viii, 4. 

Arnaud. Recherches cliniques sur la paralysie generale chez l'homme. These 
de Paris, 1888. 

Petersen-Borstel. Ueber Feldzugsparalysen. Allgem. Zeitschr. f. Psych., 1888, 
xliv, 4. 

Ritti. Gaz. hebd., 1888, 2me sen, xxv, 43, 45, 49. 



CHAPTER IV. 

SYPHILIS OF THE GENERAL NERVOUS SYSTEM. 

In different places in our book, in the chapters on diseases 
of the brain as well as in those treating of affections of the 
spinal cord, we have had occasion to point out the role which 
syphilis plays as an astiological factor in various diseases. We 
have also shown that tabes and the progressive paralysis of the 
insane are to be regarded as the main representatives of affec- 
tions of the general nervous system depending upon syphilitic 
infection. It only remains, therefore, in the present chapter 
to add some general remarks to what has already been stated. 

No part of the nervous system, whether of the brain or of 
the spinal cord, is exempt from the chance of becoming impli- 
cated in the syphilitic infection, and remembering how the 
blood-vessels are affected by syphilis this is easily understood. 
Clinically, it is especially interesting if we are able to recognize 
diseases of the cerebral cortex and symptoms — e. g., monople- 
gias — resulting therefrom, as syphilitic, but the corona radiata 
and the basal ganglia, the pons, the medulla oblongata, and the 
cerebellum, all may become the seat of syphilis, and syphilitic 
affections of the base of the brain are relatively common. In 
many cases it is difficult to make a certain diagnosis, especially 
if the patient denies the primary sore and no trace of it can be 
found, for the clinical symptoms, of course, are the same, 
whether the brain lesion depends upon syphilis or not. 

Symptoms. — Among the manifold symptoms which occur 
in brain syphilis we may mention polyuria and polydipsia (cf. 
Buttersack, lit.), but these may, it seems, occur also primarily. 
If focal symptoms are present it is easier to make a diagnosis 
than in their absence. In the latter case it may sometimes be 
impossible to decide upon the diagnosis of brain syphilis ; we 
may be dealing with a case of cerebral neurasthenia. 

With reference to the spinal cord the matter is somewhat 



SYPHILIS OF THE GENERAL NERVOUS SYSTEM. 



6 57 



more simple, because syphilitic disease here, which does not 
implicate also the brain, as in tabes and progressive paralysis 
of the insane, is rather rare. It is not a common thing- to find 
disease of one system of fibres or disease of several systems 
combined depending upon syphilis, and the cases where lateral 
sclerosis, for example, was attributed to this have been pub- 
lished as rarities. In the work of Rinecker (cf. lit.) all the ref- 
erences on this subject will be found. It is of pathological 
interest to note, as Buttersack has also pointed out, that the 
root bundles usually present a marked and extensive participa- 
tion in the process. In a case reported by Siemerling (cf. lit.) 
there were gummatous growths of the pia, which, although 
they had extended into the substance of the cord, had not at- 
tacked any " system " in its whole extent, so that, as is often the 
case, the spinal symptoms here also were not at all prominent. 

We can not assume that the spinal nerves, either motor or 
sensory, ever become diseased alone, but we must rather look 
upon their implication as a partial manifestation of a general 
affection. If in exceptional cases we find a neuritis of the 
sciatic or of the musculo-spiral nerve, etc., which we have to 
regard as of syphilitic origin, perhaps because it rapidly passes 
off under antisyphilitic treatment, the manifestations of cerebral 
and spinal syphilis have either existed previously and have not 
been recognized or their presence later has to be looked for. 

Diagnosis. — The diagnosis is based first upon the history of 
the patient and the presence of signs of the primary sore. If 
these are established, it is relatively easy ; if not, we must look 
for other signs to help us. Secondly, the other organs — for 
instance, the skin, the visible mucous membranes — all must be 
examined for the possible existence of syphilitic lesions. Re- 
peated and careful search may sometimes clear up much that 
is obscure, although the patient's account may be imperfect. 
Thirdly, it must be remembered that the symptoms of cerebral 
syphilis are extremely changeable, and are rarely ever of long 
duration. To-day, matters may look as if the patient's life 
were in danger, while to-morrow he is apparently perfectly 
safe again. The rapidity with which the changes in the con- 
dition follow each other, just as in hysteria, the extraordinary 
circumstance that apoplectiform attacks occur in younger and 
epileptiform attacks in older persons, in doubtful cases are in 
favor of the diagnosis of syphilis of the nervous system. In 
every instance we shall do well to pay careful attention to the 
42 



658 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

condition of the eyes, and be on the lookout not only for a 
possible ophthalmoplegia, but also for iritis. Finally, the thera- 
peutic test is of some value, inasmuch as the successful anti- 
syphilitic treatment makes the existence of syphilis almost 
certain, although a failure does not warrant the contrary con- 
clusion. 

Prognosis. — The prognosis must, above all, be influenced by 
the time which has elapsed since the primary infection and be- 
fore the first appearance of the nervous symptoms. The longer 
this period of incubation the worse is the prognosis. Accord- 
ing to my own experience, from five to nine years is the most 
common time. Occasionally the infection of the nervous sys- 
tem manifests itself earlier, and in quite exceptional instances 
two years, or even one year after the primary lesion ; but often 
the interval which elapses is longer than the time above given. 
Cases in which the spinal or cerebral symptoms did not appear 
till after twenty or twenty-five years I have never seen get 
well. The second question of importance is, how long the 
nervous symptoms have existed before energetic antisyphilitic 
treatment was commenced. Often as it remains without effect, 
a trial of it is still indicated if not more than two or four 
months have elapsed after their appearance. If they have 
existed for half a year or longer, nothing can be expected from 
any such treatment, and it need not, therefore, be begun. In 
such cases the prognosis, of course, is worse than in the others. 
Thirdly, a good deal depends upon the kind of symptoms by 
which the infection of the nervous system manifests itself. 
General symptoms, headache, vertigo, epileptiform attacks, 
allow, ceteris paribus, of a more favorable prognosis than focal 
symptoms, such as monoplegias, hemiplegias, and paralyses of 
certain nerves. The worst outlook is afforded by those in- 
stances in which the brain and the spinal cord are equally 
severely attacked, as in tabes and progressive paralysis of the 
insane. 

Treatment. — The manner in which the treatment is to be 
conducted must be made to depend upon the individual case, 
the age, the nutrition of the patient, and so forth, and no rule 
applicable to all cases can be laid down. Only one remark, 
which has repeatedly been made before in this book, we wish 
here again to emphasize, namely, that if we have once decided 
upon adopting the antisyphilitic treatment we must do so 
energetically, giving iodide of potassium, one to six or eight 



SYPHILIS OF THE GENERAL NERVOUS SYSTEM. 



659 



grammes (grs. xv- 3 jss.- 3 ij) daily, in one or two doses in hot 
milk, continued for from six to ten weeks, and inunctions of 
blue ointment, from three to five grammes (grs. xlv-lxxv) a 
day, continued for from four to six weeks. All necessary pre- 
cautions are self-evident. Finally, we should not neglect to 
familiarize ourselves with the progress which has been made 
in the modern treatment of syphilis, and consider whether the 
subcutaneous use of mercury is advisable, and, if so, what the 
exact mode of its administration then should be. 

LITERATURE. 

Muller. Ein Fall von Hirnsyphilis etc. Inaug. Dissert. Gottingen, 1886. 
Rumpf. Die syphilitischen Erkrankungen des Nervensystems. Wiesbaden, 

Bergmann, 1887. 
Hood. Lancet, January 4, 18S7, 1. (Syphil. meningitis.) 
Kahler. Prag. med. Wochenschr., 1886, xi, 48. (Syphilitic root neuritis.) 
Courtade. Encephale, Mars, 1887, vii. (Syphilit. aphasia.) 
Rinecker, v. Riickenmark u. Syphilis. Festschr., Leipzig, 1882. 
Buttersack. Zur Lehre von den syphil. Erkrankungen des Centralnervensys- 

tems u. s. w. Arch. f. Psych, und Nervenkr., 1886, xvii, 3, 603. 
Aikmann. Glasgow Med Journ., October 4, 1887, xxviii. 

Budor. Ann. de dermat. et syph., March 3, 1888, viii, 3. (Syphil. paraplegia.) 
Anderson. Glasgow Med. Journ., April 4, 1888, xxix. (Syphilis of the spinal 

cord.) 
Ziemssen. Syphilis des Nervensystems. Klin. Vortr., iv, November 3, 1888. 
Warrer. Brit. Med. Journ., September, 1888. (Two cases of cerebral syphilis 

in one family.) 
Bruschini. Sifilide dei centri nervosi. Rivista delle cliniche, 1888, 1. 
Jiirgens. Berl. klin. Wochenschr., 1888, xxv, 22. (Syphilis of the spinal cord.) 
Oppenheim. Berl, klin. Wochenschr., 1888, 53. 
Siemerling. Arch. f. Psych, u. Nervenkr., 1888, xx, 1. (Congenital cerebral 

and spinal syphilis.) 
Naunyn. Mittheilungen aus der medicinischen Klinik zu Konigsberg. Leipzig, 

Vogel, 1888. 
Moravsik. Centralbl. f. Nervenheilk., 1888, 20. (On hysterical symptoms in 

cerebral syphilis.) 
Regnier. Rapports de la syphilis cerebrale avec la paralysie generale. Revue 

de med., 1889, 7, 8. 
Naunyn. Die Prognose der syphilitischen Erkrankungen des Nervensystems. 

XIII. Wanderversammlung der siidwestdeutschen Neurologen. Archiv f. 

Psych, u. Nervenkr., 1889, xx, 2. 
Fischer. Boston Med. and Surg. Journ., January 3, 1889, cxx. (Brain syphilis.) 
Gowers. Lancet, January, 1889, 1, 2. 
Maurice. Gaz. des hop., 1889, 24, 33, 39. (Brain syphilis.) 



APPENDIX. 

INTOXICATION PARALYSES. 

It would be beyond the scope of this work to treat here at 
length of the pathology of the intoxication paralyses, which 
form a well-recognized part of the poisonings and the diseases 
in general due to the various trades and occupations; we only 
wish at the end of this book to point out, that working in poi- 
sons may under certain circumstances lead to diseases which 
affect the general nervous system, and which therefore can well 
be treated of here in an appendix to the preceding chapters. 

The intoxication paralyses come on either acutely or gradu- 
ally ; their symptoms and course are influenced and modified 
(a) by the nature of the poison ; {&) by the manner in which 
the poison enters the body, whether through the organs of 
respiration or digestion or through the skin, either when the 
epidermis is intact or when there is a loss of continuity in 
places. In how many ways the work itself — that is, the differ- 
ent manipulations, etc. — favor the entrance of the poison into 
the system can not here be dwelt upon. In the third volume of 
my Krankheiten der Arbeiter this subject is fully discussed. 

The substances which are here concerned are inorganic 
as well as organic; gaseous poisons may also be injurious. 
Among the inorganic substances it is especially certain of the 
heavy metals, which first attract our attention. Every year 
hundreds and thousands of people are occupied in elaborating 
them so as to adapt them for their different uses, and the num- 
ber of persons whose health is thereby damaged is consider- 
able, in spite of the measures of precaution established by law. 

The motor disturbances which develop under their influence 
are more particularly paralyses, but before the occurrence of 
these symptoms, and also during their existence, certain signs 
of motor irritation may be observed, which manifest them- 
selves frequently in tremor, or more rarely in spasm. Certain 



LEAD PALSY. 66 t 

metals — for instance, mercury — seem to be particularly apt to 
give rise to symptoms of irritation, whereas others, like arsenic 
and lead, seem more rarely to have this effect ; in cases of poi- 
soning- from the latter, symptoms of paralysis are more marked. 
Sensory disorders are rare, and only in certain intoxications — 
for instance, in lead poisoning— do they constitute an annoying 
and prominent feature of the disease. Lead, more than any 
other of these substances, it is which produces the severest 
disturbances in those who occupy themselves with it, and it is 
safe to say that the brain as well as the spinal cord and all the 
peripheral nerves are equally exposed to its injurious influence. 
Lead Palsy, the affection which interests us more than any 
other belonging to the present category, is confined chiefly to 
the extensors of the wrist and fingers, the triceps and supinator 
longus remaining exempt from the morbid process. There are 
cases in which the extensor region is intact, but in which the 
deltoid and biceps, possibly also the small muscles of the hand, 
are affected. However, the extensor paralysis alone is to be 
regarded as typical of lead poisoning. The investigations of 
Mobius more particularly, have shown that the muscles most 
exerted become affected alone, or at least more seriously than 
others. Here may also be mentioned the interesting observa- 
tion of Manouvriez, that in left-handed people the left arm is 
more affected than its fellow. As a matter of fact, both arms 
are frequently attacked to the same degree. The time at which 
the paralysis sets in varies greatly. It is very unusual for it to 
appear only a few days after exposure to the poison, and the 
case of Herard (cf. lit.), where a working man developed ex- 
tensor paralysis of both arms the same day on which he had 
filled a barrel with white lead, is decidedly unique. Usually 
some weeks elapse before the paralysis manifests itself, and 
often it is preceded by one or more attacks of lead colic. The 
course is tedious ; if the poison continues to act, the affected 
muscles undergo atrophy relatively rapidly and to a very 
marked degree, and in such cases recovery becomes improb- 
able. On electrical examination, we generally find the reac- 
tion of degeneration ; with the diminution in the number of the 
muscle fibres the excitability decreases and becomes lost com- 
pletely and forever in grave cases. The anatomical seat of 
lead palsy is unquestionably to be looked for in the peripheral 
nerves, possibly also in the muscles. It is a peripheral atrophic 
paralysis with a degeneration of the musculo-spiral and, to a 



662 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

lesser extent, of the median and ulnar nerves. In the spinal 
cord and the anterior roots, in cases oi this class, gross and 
striking changes are not demonstrable (Vierordt). Possibly 
the paralysis may also be explained by a change in the gan- 
glionic cells of the spinal cord, which takes place in conse- 
quence of the peripheral irritation in the manner lately de- 
scribed by Ssadowski in his Inaugural Dissertation (Peters- 
burg, 1889). According to his opinion, the accumulation of 
the stimuli affecting the peripheral nerves brings about an in- 
creased activity of the corresponding gangli, and with this a 
disturbance in the nutrition of the nerve cells, which leads to 
an atrophic degeneration. 

Besides the peripheral, we have also central lead palsies : (a) 
those which depend upon spinal, (b) those which depend upon 
cerebral lesions ; the former, the significance of which E. Re- 
mak more particularly has emphasized, are connected with 
diseases in the ganglionic cells in the anterior horns of the 
spinal cord, which are affected according to their anatomical 
position, so that groups of muscles are attacked which in their 
functions are connected with one another. The changes 
found in the spinal cord consist of numerous small haemor- 
rhages, particularly in the cervical enlargement, in the middle 
portions of the anterior horns, and in the existence of small 
atrophic, in places pigmented, ganglionic cells, which are often 
found to have lost their nuclei (Oeller, cf. lit.). The saturnine 
cerebral palsies manifest themselves as hemiplegias which ap- 
pear suddenly and resemble in every detail the ones described 
above (page 225 et seg.). It is not clear how their development 
should be explained. Disregarding the few cases in which the 
hemiplegia was connected with chronic nephritis and heart 
hypertrophy, the action of the poison has either to be regarded 
as giving rise to vaso-motor changes or else we must suppose 
that certain parts of the central nervous system are directly 
thrown into a state of irritation (Heubel, Malassez, Harnack). 

The sensory saturnine paralyses — e. g., the hemianesthesia 
which occasionally accompanies the hemiplegia, must also re- 
main as yet unexplained. The problem is by no means solved 
by calling this toxic hemianassthesia hysterical, and the ques- 
tion whether the group of symptoms which we call hysteria 
can ever be the consequence of the occupation of the patient, 
and more particularly the consequence of lead poisoning, must 
still remain open. Possibly various symptoms which for the 



LEAD PALSY. 



663 



sake of convenience are called hysterical, in reality depend 
upon anatomical changes. The appearance of epilepsy, and of 
eclampsia, as also of certain states of excitement associated with 
hallucinations, also of the habitual headache (encephalopathia 
saturnina), of the amblyopia with consequent amaurosis, all 
point to an affection of the entire nervous system of a degree 
which is not found in poisoning from any other inorganic sub- 
stance. 

Recent investigations have made it probable that zinc in 
which among other impurities a certain amount of lead is found 
chiefly owes its poisonous action to this latter. Pure zinc, as it 
seems, has no injurious effect upon the nervous system, and 
the cases formerly described as intoxications due to zinc 
(Schlockow, Deutsch. med. Wochenschrift, 1879, v > PP- ! 7> x 8) 
must be regarded as cases of lead poisoning (Laffter). The 
possibility that some injurious action may also be attributable 
to an admixture of copper with the zinc we have mentioned on 
a former occasion, in our work Krankheiten der Arbeiter, 
iii, 1885. 

LITERATURE. 

Remak, E. Zur Pathogenese der Bleilahmung. Arch. f. Psych, u. Nerven- 
krankh., 1875, Vl ' I - 

Lancereaux. Gaz. des hop., 1875, 67. 

Daguet. Ibid., 1876, 82. (Hemianalgesia in lead poisoning.) 

Gibert. Gaz. de Paris, 1876, 10. 

Dejerine. Gaz. de Paris, 1879, 12. 

Bernhardt. Arch. f. Psych, u. Nervenk., 1878, viii, 2. 

Monakow. Arch. f. Psych, u. Nervenk., 1880, x, p. 495. 

Junker. Zeitschr. f. klin. Med., 1880, i, p. 496. 

Samson. Etude sur la paralysie saturnine. These de Paris, 1882. 

Herard. Paralysie saturnine par contact. Gaz. des hop., 1882, 67. 

Geneuil. Bull, de therap., fevr. 1882, cii, p. 117. 

Charlier. Contribution a l'etude pathogenique du saturnisme cerebro-spinal. 
These de Paris, 1882. 

Oeller. Zur pathol. Anatom. der Bleilahmung. Munchen, 1883. 

Duplaix et Lejard. Arch, gener. de med., November, 1883. 

Lepine. Lyon med., 1883, 11. (Recovery from lead palsy.) 

Weber. De l'amblyopie saturnine. These de Paris, 1885. 

Porter. Lancet, September 19, 1885. (Encephalopathia saturnina in file- 
cutters.) 

Hardy. Gaz. des hop., 1885, 24. (Hemianaesthesia.) 

Oppenheim. Arch. f. Psych, u. Nervenkrankh., 1885, xvi, 2. 

Schultze. Arch. f. Psych, u. Nervenkrankh., 1885, xvi, 3. 

Suckling. Brit. Med. Journ., April, 1885. (Atrophy of the muscles.) 



664 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

Mobius. Centralbl. f. Nervenheilk., 1886, ix, 1. ("File-cutter's palsy.") 

Charcot. Gaz. des hop., 1886, 120. (Saturn. hemiariEesthesia.) 

Vierorclt. Arch. f. Psych, u. Nervenkrankh., 1887, xviii, 1. (Nature of lead 
palsy.) 

Putnam. Boston Med. and Surg. Journ., December 25, 1887, cxvii. (Pseudo- 
tabes as a consequence of lead poisoning.) 

Bernhardt. Pathologic der Bleilahmungen. Berl. klin. Wochenschr., 1887, 
xxiv, 41. 

Scheiber. Wiener med. Blatter, 1887, x, 2. 

Peter. Gaz. des hop., 1887, m. (Saturnism and alcoholism.) 

Duckworth. A Case of Saturnine Cachexia illustrating Paralysis of Arms and 
Legs, etc. Clin. Soc. Transact., 1887, xx, p. 266. 

Bertrand et Ogier. Ann. d'hyg., January 1, 1888, 3me ser., xix. 

Byron Bramwell. Brain, 1888, x, p. 507. (Brain symptoms after lead palsy.) 

Smith, Wood. Glasgow Med. Journ., April 4, 1888, xxix. 

Dutil. Gaz. de Paris, 1888, 7. 

Lindt, Jr. Encephal. saturn. mit todtl. Ausgange. Schweizer Correspondenz- 
bl., 1888, xviii, 9. 

Nonne u. Eisenlchr. Deutsche med. Wochenschr., 1888, xiv, 25. (Functional 
paralysis in a lead-worker cured by suggestion.) 

Dutil. Hysterie saturnine. Gaz. de Paris, 1888, 93. 

Souques. Gaz. de Paris, 1889, 2. (Hysterical hemiplegia after lead poisoning.) 

Potain. Encephal. saturnine. Gaz. des hop., 1889, 27. 



Suckling. Notes on Multiple Peripheral Neuritis and its Occurrence in Brass- 
workers. Brit. Med. Journ., December, 1888. 



Arsenical paralysis may set in from five to ten days after 
the symptoms of an acute intoxication have made their appear- 
ance, sometimes not until some weeks later. It commences 
with pains and parsesthesias in the extremities, which persist 
for a variable period of time, together with a marked weakness 
of the lower extremities, which soon makes walking and stand- 
ing difficult for the patient. The extensors are the muscles 
most seriously attacked. Dorsal flexion of the foot and the 
toes becomes difficult, the walk is pronouncedly ataxic; the 
legs are raised a good deal during walking in order to keep 
the drooping foot from touching the ground. The presence of 
Romberg's sign, together with the gait, may lead us to think 
of tabes if the history of arsenical poisoning is, for some reason 
or other, not clear. The affection of the upper extremities 
consists of paresis of the extensor muscles, of those of the 
thenar and antithenar, which, although the elbow and shoulder 
joint remain intact, gives rise to a considerable disturbance of 
function in the hands. To this motor disorder there is soon 



A R SENICA L PA RA L YSIS. 



665 



added, as we have seen to be the case in lead poisoning, a pro- 
nounced atrophy of the muscles, which is more particularly 
marked in the lower extremities, while it is less noticeable in 
the arms. The electrical excitability is here also, at least in 
the grave cases, completely lost. Vaso-motor changes do not 
occur, with the exception of occasional oedema about the 
ankles. The whole disease lasts for from a few months to 
three, four, or five years. Although complete recovery is not 
common, as a rule some improvement is noted, and the patient 
regains some movements. Arsenical paralysis may be mistaken 
more particularly for syringomyelia, for multiple neuritis, and 
for tabes; however, the history of exposure to arsenic, the 
peculiarity of the motor disturbances, which are more marked 
in the lower than in the upper extremities, the nonim plication 
of the sphincters, and the rarity with which the cranial nerves 
are attacked, will, as a rule, be sufficient to allow of a correct 
diagnosis. That the anatomical seat of the arsenical paralysis 
must be sought for in the peripheral nerves, that we are deal- 
ing with a peripheral neuritis, and more particularly with a 
toxic form in the sense of the term used by Leyden, has been 
shown by Strumpell and Falkenheim, and quite recently again 
by Alexander (cf. lit.). 

The pathogenesis is, according to the same author, to be 
connected with the fact pointed out by Silbermann (Deutsche 
medicinische Wochenschrift, 1888, p. 504), who claims that un- 
der the action of arsenic an obstruction of numerous capillaries 
can be demonstrated in the different organs, especially in the 
lungs, the gastro-intestinal tract, the liver, and the kidneys. 
Similar circulatory disturbances in the nervous system Alex- 
ander claims to be the cause of the arsenical paralysis. 

There is no doubt but that arsenic may have a noxious ac- 
tion not only upon the peripheral nerves, but also upon the 
central nervous system, although, according to the statement 
of Alexander, Scolosuboff and Popow could not find, in their 
examination, any changes in the spinal cord after arsenical 
poisoning. Pathologically, the action of arsenic upon the 
brain has not been demonstrated either, yet certain clinical 
facts seem to point to an affection of this organ also. Instances 
where workers in arsenic suffer from headache, psychical de- 
pression, apathy, and sleeplessness, although now, owing to 
the better prophylaxis, much less frequently met with, cer- 
tainly do occur, and prove that the brain may also be affected 



666 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

by the poison. Yet this influence is less marked and less con- 
stant in the case of arsenic than in that of lead. 



LITERATURE. 

Gerhardt. Sitzungsberichte der physikal.-med. Gesellsch., 1882, 7. 

Jaschke. Ueber Lahmungen nach acuter Arsenvergiftung. Inaug. Dissert. 
Breslau, 1882. 

Imbert-Gourbeyre. Des suites de l'empoisonnement arsenical. Paris, 1882. 

Scolosuboff. Paralysie arsenicale. Arch, de phys., 1884, pp. 323 et seg. 

Brissaud. Des paralysies toxiques. These d'agregation. Gaz. des hop., 1886, 
40. 

Cohn. Arch. f. Kinderheilk., 1886, vii, 6. 

Thomsen. Deutsche med. Zeitg., 1887, viii, 1. 

Dana. Brain, 1887, xxxvi, p. 456. (Pathology of arsenical paralysis.) 

Everett-Smith. Boston Med. and Surg. Journ., November 20, 1887, cxvii. 

Demuth. Ver. Bl. d. Pfalzer Aerzte, August, 1887, iii. 

Popow. Ueber die Veranderungen im Ruckenmarke des Menschen nach acuter 
Arsenikvergiftung. Virchow's Archiv, 1888, Bd. cxviii. 

Krehl. Ueber Arsenlahmungen. Deutsches Arch. f. klin. Med., 1889, xliv, 4. 

Putnam. Boston Med. and Surg. Journ., March 11, 1889, Ixx, 10. 

Falkenheim. Ueber Lahmungen nach acuter Arsenintoxication. Mittheil. aus 
d. med. Klinik in Konigsberg. Leipzig, 1888. 

Alexander. Klinische und experimentelle Beitrage zur Kenntniss der Lah- 
mungen nach Arsenikvergiftung. Habilitationsschrift, Breslau, 1889. (Con- 
tains the more important references.) 

Mercury may also give rise to paralyses, but they are far 
more uncommon and develop much more slowly and gradually 
than those due either to lead or arsenic. I have repeatedly 





Fig. 175.— Specimen of Handwriting of a Patient (hat-maker) with a Mercu- 
rial Tremor. 

seen paresis of the upper and lower extremities in those work- 
ing in quicksilver, but these did not attract the attention of the 



MERCURIAL POISONING. fifty 

observers much because they came on, without exception, dur- 
ing the presence of or even long after the first appearance of 
another symptom, which, as it were, dominated the clinical pic- 
ture, namely, the tremor. In those working in mercury this 
tremor is seen even much more frequently than the typical ex- 







H 



& < 



o 8 

g < 



s 3 
u o 

I 



tensor paralysis in lead-workers. It begins usually in the face 
or the tongue, and gradually invades the upper and then the 
lower extremities. Its grade of intensity is different in different 
cases. From a slight tremor, resembling that of paralysis agi- 



668 



DISEASES OF THE GENERAL NERVOUS SYSTEM. 



tans, every stage, up to the strongest shaking movement, even 
convulsive jerkings passing through the whole body, and simi- 
lar to those of a severe chorea, may be observed. They cease 
during sleep, but in the waking stage are aggravated by every 





^ 




movement, so that they remind one of the tremor of multiple 
sclerosis. After this has lasted for years, more or less pro- 
nounced muscular weakness appears, but paralyses without 
tremor do not occur as a result of quicksilver poisoning. Ac- 



MERCURIAL POISONING. 



669 



cording- to the investigations of Letulle (cf. lit.), we are here 
again dealing with a peripheral disease, the myeline sheath 
becoming degenerated while the axis cylinders remain intact. 
To this latter circumstance the possibility of recovery from 




mercurial tremor may be attributed. Besides the tremor there 
are seen circumscribed areas of anaesthesia and hyperaesthesia. 
The occasional amblyopias, the diminution in acuteness of 
hearing: and smell, the gradual dulling: of the intellectual facul- 



670 DISEASES OF THE GENERAL NERVOUS SYSTEM. 

ties, which may pass into pronounced dementia, all point to an 
implication of the entire nervous system. 

The belief which lately has been repeatedly expressed (Le- 
tulle, Guinon), that in connection with mercurial poisoning 
hysterical symptoms may appear, so that we should be justi- 
fied in speaking of a mercurial hysteria, must be held subject 
to this reservation, namely, that simultaneously with this in- 
toxication, hysteria may occur just as it is known to accompany 
neurasthenia, tabes, and many other nervous affections. To 
regard this, however, as a toxic hysteria which has its own pe- 
culiarities and course is, according to our opinion, unquestion- 
ably not justifiable. Hysteria will remain hysteria no matter 
whether it develops under the influence of mercury, alcohol, 
or lead, etc. If, as may be the case, speech disturbances and 
nystagmus occur in the course of mercurialism, care must be 
taken not to mistake it for multiple sclerosis. Wising (cf. lit.) 
has considered the question of the differential diagnosis be- 
tween the two. The difference between the mercurial and 
other forms of tremor with regard to the oscillations is shown 
in the specimens of handwriting which are represented in Figs. 
175 to 178, all taken from observations of my own. 

LITERATURE. 

Wising. Nord. Med. ark., 1880, xii, 3, No. 17. (Differential diagnosis between 

chronic mercurialism and multiple sclerosis.) 
Marie et Londe. Revista de la Sociedad Espagnola de Hygiene, 1884, pp. 249, 

385- 
Raymond. L'Intoxication mercurielle, aux mines d'Almaden. Progr. med., 

1884, 49. 
Charpentier. Revue d'hyg., vii, February 2, 1885. (Cerebral disturbances after 

mercury poisoning.) 
Marechal. Des troubles nerveux dans l'intoxication mercurielle lente. These 

inaug. de Paris, 1885. 
Letulle. Recherches cliniques et experim. sur les paralysies mercur. Arch, de 

phys., 1887, 3me s., ix, 3, 4. 
Guinon. Hysterie mercurielle. Gaz. de Paris, 1887, 78. 
Letulle. De l'hysterie mercurielle. Gaz. hebd., 1887, xxxiv, 38, 39. 
Kaufmann, E. Die Sublimatintoxication. Breslau, Kobner, 1888. 
Merget. Action toxique, physiol. et therapeut. des vapeurs mercurielles. These 

de Bordeaux, 1888. 
Rendu. Hysterie et intoxication mercurielle. Gaz. des hop., 1889, 30. 

Further, bisulphide of carbon must be mentioned in this 
connection, under the influence of which motor paralyses and 



ERGO TINE POISONING. 6^! 

anaesthesias have recently been observed. Certain authors have 
also designated the symptoms produced by these gases as hys- 
terical, and liave coined the name " bisulphide of carbon hys- 
teria." We have just expressed our opinion on such a con- 
ception. 

LITERATURE. 

Tamassia. Riv. sperim. di freniatr., etc., 1881, vii, 3. 

Sapelior, E. Etude sur le sulfure de carbone. Paris, 1885. 

Dujardin-Beaumetz. Gaz. des hop., 1885, 87. (Makes the sulphureted hydro- 
gen present in bisulphide of carbon responsible for the noxious action.) 

Mendel. Deutsche med. Wochenschr., 1886, xii, 26. (Paralyses after bisulphide 
of carbon poisoning.) 

Marie. Sulfure de carbone et hysteric Gaz. hebd., 1888, 2me sen, xxv, 47. 

Finally, a few words may be devoted to the highly interest- 
ing disease of the central nervous system attributable to the in- 
gestion of ergot. Clinically, as Tuczek (cf. lit.) has observed, 
the brain and spinal cord take an equal part in the affection, 
but as a rule anatomical changes in the latter only could be 
demonstrated. They were similar to those found in tabes, con- 
sisting, namely, of a degeneration of the posterior columns, so 
that we were tempted to call the disease " ergotine tabes." 
The whole course of the disease, however, which is not pro- 
gressive, and which differs greatly from that of tabes, does 
not justify this designation, which besides would only be liable 
to give rise to misunderstandings. 

LITERATURE. 

Siemens. Psychosen bei Ergotismus. Arch. f. Psych, und Nervenkrankh., 
1 88 1, xi, pp. 336 et seq. 

Tuczek. Ueber die Veranderungen im Centralnervensystem, speciell in den 
Hinterstrangen des Rii'ckenmarks. Ibid., 1882, p. 99. 

Tuczek. Ueber die bleibenden Folgen des Ergotismus fur das Centralnerven- 
system. Ibid., 1887, xviii, 2. 



INDEX. 



Abducens, anatomy of, 42 ; paralysis of, 
46 ; paralysis of, in tabes, 588 ; paralysis 
of, in tumor of brain, 297. 

Abductor paralysis, 111 ; in tabes, 592. 

Abscess of brain, 261 ; of spinal cord, 458. 

Absence in epilepsy, 539. 

Accessorius, anatomy of, 138 ; lesions of, 
in tabes, 593 ; paralysis of, 140 ; spasm 
of, 139. 

Accommodation, errors of, as a cause of 
migraine, 63. 

Acromegaly, 403. 

Adductor paralysis, 114 ; spasm, 112. 

Agraphia, 177. 

Agrypnia, 61. 

Alalia, 156. 

Alcoholic neuritis, 387. 

Alcoholism, treatment of, by suggestion, 
572. 

Alexia, 177. 

Alternating hemiplegia, 84, 205. 

Amaurosis in cerebral tumors, 295, 300. 

Amaurosis, epileptiform, 31. 

Amaurosis partialis fugax, 36. 

Amblyopias, toxic, 37. 

Amyotrophic lateral sclerosis, 441. 

Anaemia, cerebral, 255 ; spinal, 456. 

Anaesthesia in cord disease, 422. 

Anaesthesia, doll's head, 523 ; gustatoria, 
106 ; in hysteria, 512 ; laryngeal, 1 13 ; in 
transverse myelitis, 444 ; in tabes, 601 ; 
in traumatic neuroses, 523 ; of trigemi- 
nus, 73 ; in unilateral cord lesions, 450. 

Analgesia, in apoplexy, 226 ; in syringo- 
myelia, 464 ; in tabes, 603. 

Anarthria, 156. 

Aneurisms of cerebral arteries, 254 ; mil- 
iary, 216 ; of spinal arteries, 455. 

Angina pectoris, 121 ; in tabes, 593. 
43 



Angio-neurotic oedema, 128, 395. 

Angiomata of cord, 460. 

Anidrosis, 395. 

Anisocoria, 500, 589 ; in general paresis, 
647. 

Ankle clonus, 420. 

Antipyrine as a cause of epilepsy, 545. 

Anosmia, 25. 

Aphasia, amnesic, 177 ; in children, 181; 
conduction, 176 ; due to fright, 180 ; 
Grashey's, 181 ; motor, 175 ; reflex, 
181 ; sensory, 176 ; total, 176. 

Aphonia, hysterical, 509. 

Apoplectiform attacks, in hsematoma dune 
matris, 6 ; in general paralysis, 649. 

Apoplexie foudroyante, 221. 

Apoplexies, capillary, 10. 

Apoplexy, cerebral, 215; hysterical, 510; 
spinal. 452 ; spinal-meningeal, 323. 

Arachnoid, anatomy of, 4. 

Aran-Duchenne type of progressive mus- 
cular atrophy, 432. 

Arc de cercle in hysteria, 562. 

Argyll-Robertson pupil, 46, 589, 617. 

Arsenic, paralysis caused by, 664. 

Arteries, cerebral, 213 ; dilatation of, 254; 
embolism and thrombosis of, 245 ; neu- 
roses of, 255. 

Arteries, spinal, 451; dilatation of, 455; 
embolism and thrombosis of, 454. 

"Artery of cerebral haemorrhage," 215. 

Artery, middle cerebral, 213. 

Arthropathie des ataxiques, 61 1. 

Aspermatism, 499. 

Asphyxia, local, 397. 

Aspiration pneumonia in bulbar paralysis, 
158. 

Associated lateral movements of eyes, 48. 

Associated movements, 231; in tabes, 599. 



674 



INDEX. 



Asthma, bronchial, 117; cardiac, 126; hys- 
terical, 118, 509; saturnine, 118 ; thy- 
micum, 112. 

Ataxia, cortical, 184 ; functional, 622 ; 
hereditary, 437 ; locomotor, 586 ; in 
tabes, 596. 

Athetosis, 281 ; bilateral, 260. 

Atrophy, muscular ; congenital, 412 ; in 
hemiplegia, 234; hysterical, 511; myo- 
pathic, 407 ; progressive spinal, 431. 

Atrophy, optic, 32 ; congenital, 33 ; in gen- 
eral paresis, 649 ; in multiple sclerosis, 
580 ; in tabes, 587. 

Attack, apoplectic, 221 ; apoplectiform, 
due to cerebral compression, 6 ; epilep- 
tic, 535; hysterical, 514; hystero-epi- 
leptic, 561. 

Auditory nerve, anatomy of, 94 ; diseases 
of. 95. 

Aura, epileptic, 533. 

Automatisme ambulatoire, 539. 

Automatism in hystero-epilepsy, 564. 

Backache, 421. 

Basal ganglia, anatomy of, 192 ; lesions of, 

192. 
Basedow's disease, 131. 
Ballismus, 473. 

Bed-sore, acute malignant, 233. 
Beri-beri, 328. 
Birth palsy, 351. 

Bisulphide-of-carbon intoxication, 670. 
Bladder, disturbances of, in myelitis, 446 ; 

in tabes, 606 ; hyperesthesia of, 375 ; 

paralysis of, 375. 
Blepharoptosis cerebralis, 44. 
Blepharospasm, 80. 
Brachial plexus, anatomy of, 331 ; diseases 

of, 338. 
Brain abscess, 261. 
Brain syphilis, 656. 
Breast, irritable, 362. 
Bromides in epilepsy, 551. 
Bromism, 552. 

Brown-Sequard's paralysis, 450. 
Bulbar paralysis, 155 ; pseudo, 251. 
Burdach, columns of, 418. 

Cachexie exophthalmique, 131. 
Cachexie pachydermique, 398. 
Cadaveric position of vocal cords, 114. 
Capsule internal, anatomy of, 188 ; lesions 
of, 197. 



Carcinoma, of brain, 290 ; of cord, 461 ; of 

vertebrse, 447. 
Cardiac branches of vagus, 120. 
Cardialgia, 127. 
Cardiogmus juvenilis, 123. 
Caries of spine, diseases of cord in, 447 ; 

pachymeningitis spinalis due to, 313. 
Carrefour sensitif, 200. 
Catalepsy, 563. 
Cauda equina, tumors of, 462. 
Cavity formation in cord, 464. 
Centrum ovale, anatomy of, 188 ; lesions 

of, 191. 
Cephalsea, 57. 
Cephalalgia, 57. 

Cerebellar, abscess, 263, 265 ; ataxia, vide 
Equilibrium, loss of, in diseases of cere- 
bellum ; peduncles, lesions of, 20S ; 
tract direct, 418. 
Cerebellum, anatomy of, 207 ; lesions of, 

208. 
Cerebral, abscess, etc., vide Brain abscess, 
etc. ; arteries, anatomy of, 213 ; sinuses, 
258 ; veins, anatomy of, 258 ; veins, dis- 
eases of, 259. 
Cerebro-spinal meningitis, II, 14. 
Cervico-brachial neuralgia, 356. 
Cervico-occipiial neuralgia, 337. 
Charcot's joint, in tabes, 611. 
Cheyne-Stokes breathing in apoplexy, 222. 
Chiasm, optic, anatomy of, 28 ; lesions of, 

33- 
Choked disk, cf. also Papillitis, 29. 
Cholesteatoma of brain, 290. 
Chorda tympani, lesions of, 87. 
Chorea, 473 ; congenital, 479 ; electrical, 
474 ; hereditary, 479 ; Huntington's, 
479 ; imitatoria, 480 ; major and minor, 
473 ; in pregnancy, 479 ; senile, 480 ; 
Sydenham's, 473 ; symptomatic, 482. 
Circle of Willis, 213. 

Circumflex nerve, neuralgia of, 350 ; pa- 
ralysis of, 350. 
Clavus hystericus, 508. 
Claw hand, 349, 351, 432. 
Clonus, ankle, 420. 
Clownism, 562, 
Clubfoot, paralytic, 425. 
Cocaine as a cause of epilepsy, 545. 
Coccygeal nerve, anatomy of, 369. 
Coccygodynia, or Coccydynia, 376. 
Color vision, in tabes, 587 ; in hysteria, 
508. 



INDEX. 



6 75 



Coma, in cerebral hemorrhage, 221 ; dif- 
ferential diagnosis of, 234 ; epileptic, 
235- 

Commissure, optic, vide Chiasm. 

Compression myelitis, 447. 

Concussion, spinal, 522. 

Conduction aphasia, 176. 

Conduction of motion and sensation in 
cord, 418. 

Congenital diseases of brain, 305 ; of cord, 
463- 

Conjugate deviation of eyes, 48, 224. 

Contractures, in infantile cerebral palsy, 
272 ; in spinal paralysis, 426 ; in hemi- 
plegia, 229 ; in hysteria, 512, 518. 

"Contractures des nourrices," 486. 

Convergence, insufficiency of, in Graves's 
disease, 132. 

Convolutions of brain, 170. 

Convulsive tic, 78. 

Convulsions, epileptic, 535. 

Convulsions, epileptiform, in brain tumor, 
293 ; in cerebral palsy of children, 272 ; 
in childhood, 556 ; in hematoma durae 
matris, 6 ; in spinal paralysis of children, 
425- 

Convulsions, hystero-epileptic, 562 ; in- 
fantile, vide Eclampsia; puerperal, 556 ; 
uraemic, resembling Jacksonian epilepsy, 

549- 
Co-ordination, disturbances of, in tabes, 

596. 
Co-ordination of movements, 596. 
Co-ordination occupation neuroses, 353. 
Cornu Ammonis in epilepsy, 548. 
Corona radiata, 188. 
Corpora albicantia, 203. 
Corpora quadrigemina, anatomy of, 200 ; 

lesions of, 202. 
Corpus callosum, absence of, 309. 
Corpus striatum, lesions of, 251. 
Cortex cerebral, anatomy of, 169 ; lesions 

of, 172. 
Cortical areas, absolute, 168 ; relative, 168. 
Cortical, ataxia, 184 ; epilepsy, 185 ; motor 

disturbances, 182 ; sensory disturbances, 

185 ; vessels, 214. 
Cough, hysterical, 509. 
Cough, trigeminal, 75. 
Cranial nerves, diseases of, 23 ; in brain 

tumor, 297 ; implication of, in hysteria, 

507 ; in tabes, 587 ; multiple affection 

of, 150. 



Cremasteric reflex, 419. 

Crises clitoridiennes, C09. 

Crises du courbature musculaire, 600. 

Crises in tabes, 591. 

Crises vesicales, 607 ; vesico-urethrales, 
608. 

Crossed, diplopia, 48 ; pyramidal tracts, 
189, 418. 

Crura cerebri, anatomy of, 203 ; lesions of, 
204. 

Crural nerve, neuralgia of, 367 ; paraly- 
sis of, 368. 

Crusta, 188, 203. 

" Crutch palsy," 343. 

Cuneus, 171. 

Cutaneous reflexes, 419. 

Cylindroma of the cord, 461. 

Cyst, apoplectic, 217, 247. 

Cysticercus, of brain, 303 ; of spinal cord, 
463- 

Dairymaid's cramp, 355. 

Dance, St. Vitus', 473. 

Deafness, in hysteria, 507 ; in meningitis, 
20, 96 ; in tabes, 590 ; word, 174. 

Deep reflexes, 419. 

Degeneration, gray, of optic nerve, 32. 

Degeneration, of nerves, 329 ; reaction of, 
91 ; secondary, in brain diseases, 229, 
439 ; in spinal diseases, 440 ; signs of, in 
epileptics, 541. 

Deglutition paralysis, hysterical, 510. 

Delayed sensation in tabes, 603. 

Dementia in brain tumor, 294. 

Dementia paralytica, 644. 

Depression in general paralysis, 648. 

Destruction, symptoms of, 164. 

Deviation, conjugate, 48, 224. 

Diabetes, knee jerk in, 606. 

Diabetes, multiple neuritis following, 386 ; 
ataxia following, 623. 

Diabetic coma, 236. 

Diagnosis, pathological, in brain diseases, 
211. 

Diaphragm, paralysis of, 335 ; spasm of, 
335- 

Diarrhoea in tabes, 592. 

Diffuse sclerosis, cerebral, 267. 

Diffusion electrode, 72. 

Digestive disturbances connected with the 
vagus, 126. 

Diphtheria, ataxia following, 622 ; hemi- 
plegia following, 219 ; laryngeal anses- 



6y6 



INDEX. 



thesia following, 113 ; paralysis of laryn- 
geal muscles after, n 1 ; paralysis of 
pharyngeal muscles after, 151 ; neuritis 
following, 386 ; oculomotor paralysis 
following, 44. 

Diplegia, facial, 85. 

Diplopia, 45. 

Direct, cerebellar tract, 418 ; pyramidal 
tract, 418. 

Disseminated sclerosis, vide Multiple scle- 
rosis. 

Dorsal cord, diseases of, 422. 

Dorsal nerves, anatomy of, 360 ; diseases 
of, 361. 

Double images, examination for, 48. 

Double vision, 45. 

Duchenne's disease, vide Bulbar paralysis, 

155- 

Dura mater of brain, anatomy of, 3 ; hem- 
atoma of, 5 ; inflammation of, 5 ; new 
growths of, 289. 

Dura mater of spinal cord, anatomy of, 
312 ; inflammations of, 313. 

Dyspepsia, nervous, 128. 

Dysphagia, spasmodic, 129. 

Dystrophy, progressive muscular, 406. 

Ear disease, causing brain abscess, 261 ; 
causing meningitis, 11. 

Ecchymoses cutaneous, in tabes, 601. 

Echinococcus, of brain, 303 ; of spinal 
cord, 463. 

Eclampsia, 556. 

Electricity in tabes, 633. 

Embolism, cerebral, 245 ; in chorea, 478 ; 
spinal, 454. 

Encephalitis interstitialis, 650 ; nonsup- 
purative, 267 ; purulent, 261. 

Encephalocele, 309. 

Encephalomalacia, 249. 

Encephalopathy, saturnine, 256, 663. 

Enchondroma of brain, 290. 

Endarteritis, cerebralis syphilitica, 253 ; 
spinalis syphilitica, 454. 

Endocarditis and chorea, 477. 

Enuresis nocturna, 376. 

Epidemic cerebro-spinal meningitis, 14. 

Epilepsia, acetonica, 548 ; procursiva, 539. 

Epilepsie partielle sensitive, 547 ; epilepsie 
tardive (late), 540. 

Epilepsy, cortical, 185, 546 ; from fright, 
544 ; and heart disease, 548 ; Jackso- 
nian, 185, 546 ; nocturnal, 537 ; reflex, 



543 ; running, 539 ; saturnine, 548, 663 ; 

and syphilis, 542 ; traumatic, 543. 
Epileptic attack, 535 ; aura, 533 ; cry, 

535 ; vertigo, 538. 
Epileptiform convulsions, cf. Convulsions, 

epileptiform. 
Erectors of spine, paralysis of, 363. 
Ergotine tabes, 671. 
Ergotism, 671. 
Etat de mal, in epilepsy, 540 ; in hysteria, 

562. 
Ether, subcutaneous injections of, as a 

cause of musculo-spiral paralysis, 345. 
Equilibrium, loss of, in diseases of the 

cerebellum, 208. 
Equivalents, apoplectic, 223 ; epileptic, 

539 ; hemicranic, 60. 
Exophthalmic goitre, 131. 
External popliteal nerve, paralysis of, 

377- 
External rectus, paralysis of, 46. 
Eye muscles, paralysis of, 43 ; in brain 

tumor, 297 ; in meningitis, 13, 17 ; in 

tabes, 588. 
Eye symptoms in tabes, 588. 

Facial hemiatrophy, 401. 

Facial nerve, anatomy of, 77 ; central pa- 
ralysis of, 82 ; in hemiplegia, 225 ; in 
lesions of pons, 84, 205 ; peripheral pa- 
ralysis of, 86 ; spasm of, 78. 

Facies, myopathic, 409. 

Facio-lingual monoplegia, 84. 

False image, 45. 

Faradization, general, 503. 

Feeding system (Weir Mitchell), 525. 

Fifth nerve, cf. Trigeminus. 

Fissures of brain, 170. 

Flat foot, 380. 

Flexibilitas cerea, 564. 

Flexor contracture in meningitis, 14. 

Flitting scotoma, 36. 

Focal symptoms, 164. 

Foot clonus, 420. 

Forced movements, 208 ; position, 209. 

Forearm type of palsy, 429. 

Formes fnistes, in Graves' disease, 133 ; 
in multiple sclerosis, 580; in tabes, 619. 

Fothergill's face-ache, 68. 

Fourth nerve, cf. Patheticus. 

Fractures in tabes, 610. 

Friedreich's disease, 437. 

Fright and chorea, 480. 



INDEX. 



677 



Frontal lobes, 172. 
Front tap, 420. 
Functional neuroses, 471. 

Gait, in arsenical paralysis, 664 ; in multi- 
ple neuritis, 387 ; in pseudo-hyper- 
trophy, 363 ; in spastic spinal paral- 
ysis, 436 ; in tabes, 596. 

Gangrene, symmetrical, 396. 

Gasserian ganglion, 52. 

Gastralgia, 127. 

Gastric, branches of vagus, 126 ; crises, 
591 ; vertigo, 100. 

Gastrodynia, 127. 

Gastroxynsis, 62. 

General paralysis of the insane, 644 ; and 
tabes, 594. 

Gerlier's disease, 100. 

Getting up in pseudo-hypertrophy, 363. 

Giddiness, cf. Vertigo. 

Girdle sensation in tabes, 601. 

Glioma of the brain, 289. 

Glioma of spinal cord, 460. 

Gliosis in syringomyelia, 464. 

Globus hystericus, 510. 

Glosso-pharyngeal nerve, anatomy of, 
105 ; lesions of, 106. 

" Glossy fingers," 396. 

Glottis, spasm of, 112 ; hysterical, 508. 

Gluteal reflex, 419. 

Goitre, exophthalmic, 131. 

Coil's columns, 418. 

Graefe's symptom in Graves' disease, 
131 

Grand mal, 538. 

Graphospasm, 353. 

Graves' disease, 131. 

Gray matter of cord, diseases of, 422. 

Gubler's tumor, cf. Tenosynovitis. 

Gyri, cerebral, 170. 

Habit, apoplectic, 218. 

Hsematoma durse matris, 5. 

Hsematomyelia, 452. 

Hsematorrhachis, cf. Meningeal apoplexy, 

323- 
Hsematuria in tabes, 608. 
Haemorrhage, cerebral, 215 ; spinal, 452 ; 

spinal-meningeal, 323. 
Hair, falling out of, in Graves' disease, 

133 ; in hemiatrophia facialis, 401. 
Hallucinations in hysteria, 507. 
Hallucinations, state of, 564. 



Headache, 57 ; in brain syphilis, 658 ; in 
brain tumor, 292. 

Hearing, disturbances of, cf. Auditory 
nerve, 94 ; in engineers, 97 ; in facial 
paralysis, 86. 

Heart, affections of, in vagus lesions, 121 ; 
in exophthalmic goitre, 131. 

Heart disease, and cerebral haemorrhage, 
219; and chorea, 477 ; and embolism, 
246. 

Height dizziness, 101. 

Hemianesthesia, in diseases of internal 
capsule, 200, 229; hysterical, 510; 
saturnine, 662 ; in syringomyelia, 464. 

Hemianopia, 33 ; in cerebral syphilis, 35. 

Hemiataxia in cerebral apoplexy, 231. 

Hemiathetosis, 284. 

Hemiatrophia facialis, 401 ; lingualis, 
146. 593- 

Hemiatrophy in cerebral palsy of chil- 
dren, 273. 
I Hemichorea, 473 ; posthemiplegic, 231 ; 
praehemiplegic, 220. 

Hemicrania, 58 ; adolescentium, 63. 

Hemiopia, 33. 

Hemiplegia, alternans, 84, 205 ; cerebral, 
226 ; direct, 227 ; in general paralysis, 
649 ; in hsematoma durae matris, 6 ; hys- 
terical, 236, 510; indirect, 227; infan- 
tile spastic, 271 ; in lead poisoning, 219, 
662 ; spinal, 450, 453 ; in tabes, 595. 

Hemiparesis, 226. 

Hemispasm, glosso-labial, 81, 511. 

Hereditary, ataxia, 437 ; chorea, 479. 

Herpes labialis, 14 ; zoster, 361. 

Hiccough, 336. 

Hip, spastic contraction of, 384. 

Homonymous, diplopia, 48 ; hemianopia, 
34- 

Huntington's chorea, 479. 

Hydrocephalic cry, 15. 

Hydrocephalus, congenitus, 306 ; ex vacuo, 
309 ; idiopathic, 308 ; internal, 9. 

Hydromyelia, 464. 

Hydrorrhachis, 463. 

Hyperacusis in facial paralysis, 87. 

Hyperaemia of brain, 255 ; of cord, 455. 

Hyperesthesia, of auditory nerve, 95 ; in 
Brown-Sequard's paralysis, 450 ; laryn- 
geal, 113 ; in meningitis, 13 ; in tabes. 
601. 

Hyperemesis nervosa, 129. 

Hyperidrosis, 395. 



678 



INDEX. 



Hyperkinesis cordis, 123. 

Hypertrophic pachymeningitis, 314. 

Hypertrophy of muscles, 410. 

Hypnotism, 563. 

Hypoglossal nerve, anatomy of, 142 ; pa- 
ralysis of, 143 ; in hemiplegia, 225 ; 
spasm of, 148. 

Hysteria in the male, 519 ; nature of, 519. 

Hysterical, aphonia, 509 ; asthma, 509 ; 
convulsions, 514; hemianesthesia, 510 ; 
hemiplegia, 236, 510; ischuria, 514; 
neuralgia, 513 ; paralysis, 510, 511 ; 
vomiting, 510. 

Hystero-epilepsy, 561. 

Hysterogenic zones, 513. 

Imitation epilepsy, 544. 

Inequality of pupils, vide Anisocoria, 500, 
589, 647. 

Infantile, cerebral palsy, 268 ; convulsions, 
vide Eclampsia, 556 ; hemiplegia, 271 ; 
spinal paralysis, 424. 

Infraorbital neuralgia, 69. 

Insanity, post-epileptic, 536 ; prae-epilep- 
tic, 533- 

Insomnia, treatment of, 62. 

Insula, 172. 

Insular sclerosis, cf. Multiple sclerosis. 

" Insult," apoplectic, 221. 

Intention tremor, 578. 

Intercostal neuralgia, 361. 

Intermeningeal haemorrhage, 5. 

Internal capsule, anatomy of, 188 ; le- 
sions of, 197. 

Internal popliteal nerve, 380. 

Involuntary movements in tabes, 599. 

Irritable breast, 362. 

Irritable testicle, 367. 

Ischuria in hysteria, 514. 

Jacksonian epilepsy, 184, 546. 
Jaw-jerk, 441. 

Joint, Charcot's, in tabes, 611. 
Joint, hysterical, 513. 
Joint-neuralgias in hysteria, 513. 
Juvenile muscular atrophy, 407. 

Kak-ke, 328. 

Knee-jerk, 419 ; center for, 420 ; in hemi- 
plegia, 229, 233 ; in hereditary ataxia, 
437 ; in multiple neuritis, 388 ; in tabes, 
606. 

Kyphosis, 363. 



Labio-glosso-laryngeal paralysis, 155. 
Lachrymation, transient, in tabes, 588. 
Lancinating pains in tabes, 601. 
Landry's paralysis, 459. 
Laryngeal, crises in tabes, 592 ; paralysis 

in diphtheria, 111. 
Laryngismus stridulus, 112. 
Laryngospasmus, 112. 
Larynx, anaesthesia of, 113 ; nerve supply 

of, no; paralysis of muscles of, in; 

spasm of muscles of, 112. 
Late rigidity, 229. 
Lateral movements, associated, of eyes, 

48. 
Lateral sclerosis, 436 ; amyotrophic, 441. 
Laughing fits in hysteria, 509. 
Lead palsy, 344, 661, 662. 
Lead poisoning, 661. 
Lenticulo-optic artery, 215. 
Lenticulo-striate artery, 215. 
Leptomeningitis, cerebral, 9 ; spinal, 319. 
Lethargy in hysteria, 564. 
Leucomyelitis, 435. 
Levator palpebrae, paralysis of, cf. Ptosis, 

44, 589- 
Lightning as a cause of traumatic neuroses, 

522. 
Lightning pains in tabes, cf. Lancinating 

pains. 
Lipoma of brain, 290. 
Localization, cerebral, 165 ; of spinal-cord 

lesions, 421. 
Locomotor ataxia, 586. 
Lumbago, 413. 

Lumbar cord, lesions of, 422. 
Lumbar nerves, anatomy of, 363 ; lesions 

of, 367. 
Lumbo-abdominal neuralgia, 367. 

Magnet, treatment with, 563. 

Main-en-griffe, 349, 351, 432. 

Major hysteria, vide Hystero-epilepsy, 
561. 

Mai perforant du pied, 610. 

Malum Cotunnii, 369. 

Maniacal exaltation in dementia paralyt- 
ica. 647. 

Mastodynia, 362. 

Mastication, paralysis of muscles of, 55 ; 
spasm of, 54. 

Median nerve, paralysis of, 347. 

Medulla oblongata, anatomy of, 209 ; le- 
sions of, 210. 



679 



Meniere's disease, 101. 

Meningeal apoplexy, spinal, 323. 

Meninges of brain, anatomy of, 3 ; dis- 
eases of, 4. 

Meninges of cord, anatomy of, 312 ; dis- 
eases of, 313. 

Meningitis, basilar, 10 ; cerebro-spinal, II, 
14 ; gummatous, 10 ; and pneumonia, 
12 ; purulent, 9 ; tuberculous, 10, 15 ; 
spinal, 319. 

Mercurial poisoning, 666 ; tremor, 667. 

Meteorismus hystericus, 510. 

Middle cerebral artery, 214. 

Migraine, 58 ; ophthalmic, 60. 

Miliary aneurisms, 216. 

Mimic facial spasm, 78. 

Mind blindness, vide Psychical blindness, 
174. 

Mind deafness, vide Word deafness, 174. 

Miner's nystagmus, 50. 

Minor hysteria, vide Hysteria. 

Mogigraphia, 353. 

Monocontracture, 184. 

Monoparesis, 182. 

Monoplegia, cortical, 182 ; facial, 83, 199 ; 
facio-lingual, 84. 

Morbus Basedowii, 131 ; sacer, 532. 

Motor aphasia, 175 ; convolutions, 172. 

Motor oculi, vide Oculo-motorius, 40. 

Motor points, of arm, 345, 348-351 ; of 
face and neck, 92, 352 ; of leg, 379, 380. 

Multiple, neuritis, 385 ; sclerosis, 576. 

Muscles, absence of certain, 412. 

Muscular, atrophies, vide Atrophy mus- 
cular ; rheumatism, 412; sense in tabes, 
598. 

Musculo-cutaneous nerve, lesions of, 349. 

Musculo-spiral nerve, paralysis of, 342 ; 
in lead poisoning, 661 ; spasm of, 345. 

Mutism, hysterical, 509. 

Myalgia, 412. 

Myalgia, intercostal, 413 ; lumbar, 413. 

Myelitis, cervical, 422 ; chronic, 460 ; dor- 
sal, 422 ; lumbar, 422 ; purulent, 458 ; 
transverse, 443. 

Myelomalacia, 454. 

Myoclonia congenita, 512. 

Myoclonus multiplex, vide Myoclonia con- 
genita, 512. 

Myopathic facies, 409. 

Myopathies, 406. 

Myopathy, progressive atrophic, 409. 

Myosis spinal, 46 ; in tabes, 589. 



Myotonia congenita, 487. 
Myxcedema, 398. 

Nails, falling out of, in tabes, 610. 

Nerve stretching in tabes, 636. 

Nictitans, spasmus, 79. 

Nicotine poisoning, 125, 501. 

Night palsy, 396. 

Neuralgia, crural, 367 ; hysterical, 513 ; 
infra-orbital, 69 ; occipital, 337 ; sciatic, 
369 ; spermatic, 367 ; supra-orbital, 69 ; 
trifacial, vide Trigeminal, 68. 

Neurasthenia, 497. 

Neuritis, alcoholic, 387 ; arsenical, 664 ; 
infectious, 386 ; migrans, 328 ; mul- 
tiple, 385 ; nodosa, 328 ; optic, cf. Papil- 
litis, 29 ; optic, in meningitis, 14 ; retro- 
bulbar, 31 ; saturnine, 661 ; toxic, 386. 

Neuro-fibroma plexiforme, 329. 

Neuroma, 329. 

Neuro-paralytic ophthalmia, cf. Ophthal- 
mia paralytica, 73. 

Neuroses, traumatic, 523. 

Nocturnal epilepsy, 537 ; vertigo, 98. 

Nystagmus, 49 ; in Friedreich's disease, 
437 ; in multiple sclerosis, 578. 

Obturator nerve, paralysis of, 368. 

Occipital, lobe, lesions of, 174 ; neuralgia, 
337- 

Ocular vertigo, 45, 99. 

Oculo-motor nerve, anatomy of, 40 ; lesions 
of, 43 ; paralysis of, 44. 

Occupation neuroses, 353. 

(Edema, angio-neurotic, 128, 395. 

OZsophagismus, 129. 

Olfactory center, 25 ; nerve, anatomy of, 
24 ; lesions of, 25. 

Ophthalmia paralytica, 73. 

Ophthalmoplegia, progressiva, 154 ; ex- 
terna and interna, 46. 

Optic, atrophy, vide also Atrophy, optic, 
32 ; center, 29 ; chiasm, 28 ; nerve, anat- 
omy of, 28 ; nerve, diseases of, 29 ; neu- 
ritis, vide also Papillitis, 29 ; neuritis, 
retrobulbar, 31 ; radiation, anatomy of, 
29 ; lesions of, 34 ; thalamus, 29 ; lesions 
of, 195 ; tract, 29. 

Osteo-sarcoma of brain, 289. 

Otitis media as a cause of, brain abscess, 
261 ; meningitis, II. 

Ovarian hyperesthesia, 513. 

Oxyacoia in facial paralysis, 87. 



68o 



Pachymeningitis, cerebral, 5 ; cervicalis 
hypertrophica, 314 ; interna hsemor- 
rhagica, 5 ; spinalis, 313. 

Pains, lancinating, in tabes, 601. 

Palatal muscles, innervation of, 151. 

Palate, paralysis of, 151. 

Palpitation of the heart, 123. 

Papillitis, 29 ; in brain abscess, 263 ; in 
brain tumor, 295 ; in meningitis, 13. 

Papillo-retinitis, 30. 

Paracusis Willisii, 97. 

Paradoxical contraction, 421. 

Paresthesia in tabes, 602. 

Paralysis, acute ascending, 459 ; agitans, 
489; bulbar, 155; glosso-labio-laryn- 
gea, 155 ; glosso-labio-pharyngea cere- 
bralis, 251 ; hysterical, 510, 511 ; Lan- 
dry's, 459 ; post-diphtheritic, 151 ; pseu- 
do-bulbar, 251 ; spastic spinal, 436. 

Paralytic attacks, 649. 

Paramyoclonus multiplex, 512. 

Paraplegia, ataxic, 438 ; dolorosa, 462. 

Parasites of brain, 303 ; of spinal cord, 
462. 

Parietal lobes, 173. 

Parkinson's disease, 489. 

Patellar reflex, vide also Knee-jerk, 419. 

Patheticus, anatomy of, 41 ; lesions of, 
46. 

Pathological diagnosis of brain disease, 
211. 

Peduncles of cerebellum, 208. 

Peduncles, cerebral, anatomy of, 203 ; le- 
sions of, 204. 

Perforating ulcer of foot, 610. 

Periarteritis cerebralis, 215. 

Perimetric examination, 36. 

Peripachymeningitis spinalis, 313. 

Peroneal paralysis, vide External popliteal 
paralysis, 377. 

Petit mal, 538. 

Pharyngeal muscles, paralysis of, 151. 

Phonic paralysis, 114. 

Phrenic nerve, neuralgia of, 336 ; paral- 
ysis of, 335 ; spasm of, 335. 

Pia mater, cerebral, 4 ; spinal, 312. 

Pianoforte-players' cramp, 354. 

Pineal gland, tumor of, 296. 

Pitres-Nothnagel sections, 196. 

Pituitary body, tumor of, 296, 297. 

Plantar hyperesthesia, 374. 

Plantar reflex, 419. 

Plaques jaunes, 247. 



Plexus, brachial, anatomy of, 331 ; le- 
sions of, 338. 

Plexus, cervical, anatomy of, 329 ; lesions 
of, 335- 

Plexus, lumbar, anatomy of, 363 ; lesions 
of, 366. 

Plexus, sacral, anatomy of, 368 ; lesions 
of, 369. 

Pneumogastric nerve, vide Vagus. 

Points douloureux in tic douloureux, 69. 

Points, tender, in intercostal neuralgia, 
361 ; in sciatica, 371 ; in trigeminal 
neuralgia, 69. 

Polioencephalitis (Striimpell), 268 ; (Wer- 
nicke), 153. 

Poliomyelitis anterior acuta, 424 ; chron- 
ica, 429. 

Polyaesthesia in tabes, 603. 

Polydipsia in brain syphilis, 656. 

Polyneuritis, vide Multiple neuritis, 385. 

Polyuria in brain syphilis, 656. 

Polyuria, after cerebral apoplexy, 225 ; in 
hysteria, 514; in meningitis, 14. 

Pons, anatomy of, 204 ; lesions of, 205 ; 
lesions of, in facial paralysis, 84, 205. 

Popliteal nerves, 377, 380. 

Porencephaly, 267, 309. 

Post-diphtheritic paralysis, 151. 

Post-epileptic insanity, 536. 

Posterior fossa, tumors of, 297 ; sclerosis, 
vide Tabes. 

Pott's disease, 447. 

Prse-epileptic insanity, 533. 

Pregnancy, ataxia following, 622. 

Pressure myelitis, 447. 

Pressure points in blepharospasm, 80. 

Primary deviation of eyes, 47. 

Processus vermiformis of cerebellum, 207. 

Progressive, bulbar paralysis, 155 ; mus- 
cular atrophy, 431 ; ophthalmoplegia, 
154 ; paralysis of the insane, 644. 

Prosopalgia, 68. 

Propulsion, 493. 

Psammoma of brain, 290. 

Pseudo-apoplexy, 223, 257. 

Pseudo-bulbar paralysis, 251. • 

Pseudo-hypertrophy of muscles, 410. 

Pseudo-meningitis hysterica, 19. 

Pseudo-tabes peripherica, 386. 

Psychical blindness, 174; deafness, vide 
Word-deafness, 174. 

Psychical condition, after apoplexy, 230 ; 
in brain tumor, 293. 



INDEX. 



68 1 



Psychoses in tabes, 593. 

Ptosis, 44 ; in tabes, 589. 

Puerperal, convulsions, 556 ; eclampsia, 556. 

Pulmonary branches of vagus, 116. 

Pulse, in brain tumor, 294 ; in meningitis, 

13 ; slowing of, in lesions of cervical 

cord, 422. 
Pulvinar, 29, 34, 195. 
Pupil, Argyll-Robertson, 46 ; see also loss 

of light reflex in tabes, 589 and 617. 
Pupil, inequality of, vide Anisocoria. 
Pupillary reaction, 45 ; hemianopic, 34. 
Pupils in apoplexy, 221. 
Pyramidal tracts, anatomy of, 189, 418. 

Quadrigeminal bodies, anatomy of, 200 ; 

lesions of, 202. 
Quinine as a cause of amblyopia, 38. 
Quinine in Meniere's disease, 103. 

Radial paralysis, vide Musculo-spiral 
paralysis, 342. 

Railway spine, 522. 

Raynaud's disease, 396. 

Reaction of degeneration, 91. 

Rectal symptoms in tabes, 609. 

Rectum, centre for, 421. 

Recurrent laryngeal paralysis, III. 

Reflex, abdominal, 419 ; arc, 419 ; cre- 
masteric, 419 ; epilepsy, 543 ; gluteal, 
419 ; patellar, in multiple neuritis, 388 ; 
in tabes, 605 ; periosteal, 441 ; plantar, 
419 ; retained in tabes, 605. 

Reflex saltatory spasm, 384 ; tendo Achil- 
lis, 420. 

Reflexes, deep and superficial, 419. 

Relation of cortex to skull, 173. 

Respiratory organs, diseases of, in lesions 
of vagus, 116 ; innervation of, 116. 

Rest cure, vide Feeding system, 525. 

Retropulsion, 493. 

Rheumatic, acusticus paralysis, 96 ; facial 
paralysis, 89. 

Rheumatism and chorea, 476. 

Rheumatism, muscular, 412. 

Rhythmical spasm in hysteria, 518. 

Rickets and laryngismus stridulus, 112. 

Rigidity of muscles in paralysis agitans, 
491. 

Rinne's test, 103. 

Romberg's sign in tabes, 597. 

Root zone, 418, 604. 

Ructus hystericus, 510. 



Sacral nerves, anatomy of, 368 ; lesions 
of, 369- 

Salivary secretion, in facial paralysis, 86 ; 
in bulbar paralysis, 157. 

Saltatory reflex spasm, 384. 

Sarcoma of brain, 289 ; of cord, 460. 

Scanning speech, 578. 

Scar, apoplectic, 217. 

Scarlet fever, multiple neuritis following, 
386. 

Sciatica, 369. 

Sciatic nerve, anatomy of, 368 ; neuritis 
of, 369 ; paralysis of, 380. 

Sclerodactyly, 396. 

Scleroderma, 398. 

Sclerose en plaques, 576. 

Sclerosis, amyotrophic lateral, 441 ; com- 
bined posterior and lateral, 437 ; diffuse 
cerebral, 267 ; disseminated, 576 ; lat- 
eral primary, 436 ; lobar, 268 ; mul- 
tiple, 576 ; posterior spinal, 586. 

Scoliosis, 363. 

Seborrhcea, 395. 

Secondary, deviation of eyes, 47 ; lesions 
of white columns of cord, 439. 

Secretions, cutaneous, disturbances of, 
395- 

Senile, chorea, 480 ; softening, 247 ; tre- 
mor, 495, 669. 

Sensation, cortical area for, 174. 

Sensibility, examination of, in tabes, 602. 

Sensory, aphasia, 176 ; conduction in cord, 
418 ; cross way, vide carrefour sensitif, 
200. 

Sensory disturbances, in apoplexy, 230 ; 
cortical, 185 ; in peripheral nerve le- 
sions, 334 ; tabetic, 600. 

Serratus paralysis, 338. 

Sexual functions, disturbances of, in neu- 
rasthenia, 498 ; in tabes, 609. 

Shaking palsy, 489. 

Shoulder-arm palsy (Erb), 352, 

Shoulder muscles, paralysis of, 140 ; spasm 
of, 139. 

Simulation in epilepsy, 549. 

Singultus, 336; hystericus, 510. 

Sinus thrombosis, 259. 

Sinuses, cerebral, 258. 

Sixth nerve, vide Patheticus. 

Sleep, hysterical, 507. 

Sleep palsy, 344. 

Sleeplessness, causes of, 61 ; treatment of, 
62. 



682 



INDEX. 



Smell, centre for, 25 ; disturbances of, 25 ; 
examination of, 27. 

Softening, cerebral, 247 ; multiple foci of, 
in brain, 250 ; spinal, 454. 

Somnambulism, 571. 

Soul blindness, vide Psychical Blindness, 
174. 

Spasm, bronchial, 117; of glottis, 112; 
saltatory reflex, 384. 

Speech, cortical centre for, 175 ; in de- 
mentia paralytica, 647 ; disturbances 
of, vide Aphasia and special forms ; in 
Friedreich's disease, 437 ; scanning, 578. 

Sphincters, disturbances of, in cord dis- 
ease, 446 ; in tabes, 606. 

Spina bifida, 465. 

Spinal accessory nerve, vide Accessorius. 

Spinal, apoplexy, 452 ; epilepsy, 420 ; hemi- 
plegia, 450 ; irritation, 456 ; leptomen- 
ingitis, 319 ; muscular atrophy, 431 ; 
pachymeningitis, 313 ; paralysis, acute 
ascending, 459 ; paralysis, Brown-Se- 
quard's, 450 ; paralysis of children, 424 ; 
paralysis, spastic, 436. 

Spinal cord, abscess of, 458 ; anatomy of, 
417 ; blood supply of, 451 ; compres- 
sion of, 447 ; concussion of, vide Trau- 
matic neuroses, 522 ; congenital dis- 
eases of, 463 ; haemorrhage into, 452 • 
parasites of, 462 ; softening of, 454 ; 
syphilis of, 454 ; tumors of, 461. 

Spondylarthrocace, 447. 

Spondylitis, tubercular, 447. 

Status epilepticus, 540. 

Stellwag's symptom in Graves' disease, 

131- 

Stenocardia, 121. 

Sterno-cleido-mastoid, paralysis of, 140 ; 
spasm of, 139. 

Stomach, affections of, connected with va- 
gus, 126. 

Strabismus, 45. 

Stratum zonale thalami, 29. 

Stroke, apoplectic, 221 ; in cerebral em- 
bolism, 248. 

Suggestion, hypnotic, 565. 

Superior oblique muscle, 46. 

Superior peduncles of cerebellum, decus- 
sation of, 201. 

Surgical treatment, of abscess, 266 ; of 
tumors, 302. 

Suspension method in tabes, 636. 

Sydenham's disease, vide Chorea. 



Sylbenstolpern, 647. 

Syllable stumbling, 647. 

Syncope and apoplexy, 234. 

Syphilis, of brain, 656 ; and dementia para- 
lytica, 645 ; of entire nervous system, 
656 ; of spinal cord, 454 ; and tabes, 629. 

Syphilitic ophthalmoplegia, 658. 

Syphiloma of brain, 290. 

Syphiloma of cord, 461. 

Syringomyelia, 464. 

System disease, combined, 437. 

System diseases of spinal cord, 435. 

Tabes, and alcoholism, 387 ; dorsalis, 586 ; 

ergotine, 671 ; pseudo-, 386. 
Tabetic foot, 612. 
Taches cerebrales, 15, 132. 
Tachycardia, 124 ; strumosa exoph thai- 
mica, 131. 
Tailor's cramp, 355. 
Talipes, in infantile palsy, vide Clubfoot, 

425 ; in peroneal palsy, 380. 
Taste, sense of, disturbances of, in facial 

paralysis, 87 ; examination of, 106. 
Teeth, falling out of, in tabes, 610. 
Tegmentum, 203 ; lesions of, 204. 
Telegrapher's cramp, 355. 
Temporal hemianopia, 34. 
Temporal lobe, lesions of, 174. 
Temporo-sphenoidal lobe, vide Temporal 

lobe, 174. 
Tender points in tic douloureux, 69. 
Tendon reflexes, 419. 
Tenosynovitis in wrist-drop, 343. 
Terminal arteries, 214. 
Testicle, neuralgia of, 367. 
Tetanilla, 484. 
Tetanus intermittens, 484. 
Tetany, 484. 
Thalamus, optic, anatomy of, 29 ; lesions 

of, 195. 
Third nerve, vide Oculo-motor nerve. 
Thomsen's disease, 487. 
Thoracic nerve, anterior. 341 ; posterior, 

338. 
Thrombosis, cerebral, 245 ; sinus, 259 ; 

spinal, 454 ; venous, 259. 
Thyroid gland, in Graves' disease, 131. 
Tibial nerve, vide Internal popliteal. 
Tic convulsif, 78 ; douloureux, 68 ; rota- 

toire, 139. 
Tinnitus aurium, 96. 
Tobacco amblyopia, 37. 



68 3 



Tongue, atrophy of, 147 ; hemiatrophy of, 
146, 593 ; paralysis of, 144 ; spasm of, 
148. 

Torticollis, 139; rheumatica, 413. 

Tract, direct cerebellar, 418 ; optic, lesions 
of, 33- 

Tracts, crossed pyramidal, 418 ; direct py- 
ramidal, 418. 

Transverse myelitis, 443. 

Trapezius, paralysis of, 140 ; spasm of, 

139- 

Traumatic neuroses, 523. 

Traumatism and tabes, 629. 

Tremor, alcoholic, 495, 667 ; in Graves' 
disease, 133 ; mercurial, 666 : in multi- 
ple sclerosis, 578 ; in paralysis agitans, 
489 ; post-hemiplegic, 232 ; senile, 495, 
669 ; in tabes, 599, 600. 

Trigeminal cough, 75. 

Trigeminus, anaesthesia of, 73 ; anatomy 
of, 52. 

Trigeminus, central lesions of, 54 ; extra- 
cranial lesions of, 68 ; intracranial le- 
sions of, 57 ; peripheral lesions of, 56 ; 
neuralgia of, 68 ; nuclei of, 52 ; paralysis 
of, 73- 

Trochlears, vide Patheticus. 

Trophic disturbances, in cerebral apoplexy, 
233 ; in chorea, 477 ; in syringomyelia, 
465 ; in tabes, 609. 

Trophic nerves, disturbances of, 393. 

Trousseau's, sign in tetany, 484 ; spots in 
meningitis, 15. 

Tubercle of brain, 290. 

Tubercle of spinal cord, 461. 

Tubercular, disease of spine, 447 ; menin- 
gitis, 10, 15. 

Tumors, of brain, 288 ; of spinal cord, 
460; of spinal meninges, 325. 

Twitchings, fibrillary, in chronic muscular 
atrophy, 43; ; in neurasthenia, 501. 

Ulcer, perforating, 610. 

Ulnar nerve, anatomy of, 346 ; paralysis 

of, 348 ; neuralgia of, 349. 
Unilateral lesions of cord, 450. 



Upper-arm type of palsy, 429. 
Uraemia and apoplexy, 235. 
Uraemia, and epilepsy, 548 ; and Jackso- 
nian epilepsy, 549. 

Vagus, anatomy of, 108 ; lesions of, 108. 

Valleix's points, 69. 

Variola, multiple neuritis following, 386 ; 
myelitis following, 447. 

Vaso-motor nerves, 393. 

Veins, cerebral, anatomy of, 258; cerebral, 
diseases of, 259 ; spinal, 452. 

Venesection in apoplexy, 239. 

Vermiform process of cerebellum, 207, 208. 

Vermis of cerebellum, 207, 208. 

Vertebral artery, aneurism of, 254. 

Vertigo, 98; epileptic, 538; Meniere's, 101; 
in multiple sclerosis, 578, 580; ocular, 
45, 99 ; paralyzing, 100. 

Visual centre, 29. 

Visual field, contraction of, in hysteria, 
508; contraction of, in tabes, 587 ; con- 
traction of, in traumatic neuroses, 523 ; 
erroneous projection of, 45 ; examina- 
tion of, 35. 

Vocal cords, paralysis of, III; spasm of, 
112. 

Vomiting, in brain tumor, 295 ; cerebellar, 
208 ; cerebral, 13 ; in Graves' disease, 
133 ; hysterical, 510. 

Weir-Mitchell treatment, 525. 
Westphal's sign in tabes, 606. 
White substance of cord, 417, 435. 
Willis, circle of, 213. 
Word, blindness, 174; deafness, 174. 
Wrist-drop, 342; vide also Extensor paral- 
ysis in saturnine intoxication, 662. 
Writer's cramp, 353. 
Writing, disturbances of, 177. 
Wryneck, 139. 

Zinc intoxication, 663. 

Zonal stratum, vide Stratum zonale, 29. 

Zones, hysterogenic, 513. 

Zoster, herpes, 361. 



THE END. 



A TREATISE ON 
THE DISEASES OF THE 

NERVOUS SYSTEM. 

By WILLIAM A. HAMMOND, M. D., 

Surgeon-General U. S. Army (retired list). 

With the Collaboration op GRAEME M. HAMMOND, M. D., 

Professor of Diseases of the Mind and Nervous System in the New York 
Post-Graduate Medical School and Hospital, etc. 

With 118 Illustrations. 
NINTH EDITION, WITH CORRECTIONS AND ADDITIONS. 



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THE PRINCIPLES AND PRACTICE 
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By WILLIAM OSLER, M. D., 

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work "he has done in the past. If there were one fault of which we would complain, it is 
expressed in the wish that be had said more than he has. Everywhere throughout the work 
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observation, and is marked by an enlightened conservatism. It would be difficult to select 
anyone section and say that it is much better than the others. All are conspicuous for their 
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heartily commend his ' Practice of Medicine ' to those who desire to be in pi 
most recent and best knowledge on the subject with which it has to dcal."- 

" This volume exhibits originality at the very beginning, inasmuch as there is no preface. 
The author does not take us into his confidence as to his motive for adding another book on 
the 'Principles and Practice of Medicine' to those which have preceded his. He does not 
tell us whether it is because there were too many good ones or too many bad ones ; whether 
the publisher tempted him, or his university demanded it; or whether 'it was simply that he 
had noticed that ' they all do it.' He skips into the public presence without a word, but 
with a sort of air which suggests : ' Here I am ! Take me, or leave me, but you had better 
do the former ! ' He had probably heard that good wine needs no bush ; and as he has written 
a good book, with an excellent dedication and some sound aphorisms from the Greek on the 
first sheet, it mattered less about his motives. At any rate, after the table of contents and a 
list of charts and illustrations, we find ourselves plunging immediately into typhoid fever, 
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1,080 pages. No preliminaries are devoted to such abstract subjects as nosology, 
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same time animated. The type is very good. The finish of the paper is excellent, but the 
texture is not strong, and we doubt whether it stands well the strain of the eagar student 
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much as possible to necure handiness without sacrificing even more important essentials. We 
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A TREATISE ON INSANITY, IN ITS 
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instinct, sleep, dreams, and many other factors. 

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and with a degree of thoroughness which can not but lead to important results in the study 
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and abnormal standpoint. To a great extent the work relates to those species of mental de- 
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"... The times are ripe for a new work on insanity, and Dr. Hammond's great work will serve 
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hesitancy in* commending the book to the medical profession, as it is to them it is specially 
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These lectures have been reported in full, and, together with the histories of the cases, 
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to contain many of the more important affections of the kind that are commonly met with 
in practice. 

As these lectures were intended especially for the benefit of students, the author has con- 
fined himself to a full consideration of the symptoms, causes, and treatment of each affec- 
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TEXT-BOOK OF HUMAN 
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For the Use of Students and Practitioners of Medicine. 
By AUSTIN FLINT, M. D., LL D., 

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editions, the work is new in all its features. The form and typography have been 
changed. Many old figures have been expunged, and numerous new ones have been in- 
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physiological chemistry has been omitted as far as practicable. The new book is there- 
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of established facts." — Physician and Surgeon. 

" This is the fourth edition of Flint's popular text-book on physiology, entirely re- 
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a new edition be issued. The same general arrangement is preserved, and with reason. 
The beauty of Flint's Physiology consists in the exactness with which the author has 
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